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David W Hoskin - One of the best experts on this subject based on the ideXlab platform.
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Piperine an alkaloid from black pepper inhibits growth of human colon cancer cells via g1 arrest and apoptosis triggered by endoplasmic reticulum stress
Molecular Carcinogenesis, 2015Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, Melanie Power R Coombs, David W HoskinAbstract:Piperine, a piperidine alkaloid present in black pepper, inhibits the growth of cancer cells, although the mechanism of action is not well understood. In this study, we show that Piperine (75–150 µM) inhibited the growth of several colon cancer cell lines but had little effect on the growth of normal fibroblasts and epithelial cells. Piperine inhibited HT-29 colon carcinoma cell proliferation by causing G1 phase cell cycle arrest that was associated with decreased expression of cyclins D1 and D3 and their activating partner cyclin-dependent kinases 4 and 6, as well as reduced phosphorylation of the retinoblastoma protein and up-regulation of p21/WAF1 and p27/KIP1 expression. In addition, Piperine caused hydroxyl radical production and apoptosis that was partially dependent on the production of reactive oxygen species. Piperine-treated HT-29 cells showed loss of mitochondrial membrane integrity and cleavage of poly (ADP-ribose) polymerase-1, as well as caspase activation and reduced apoptosis in the presence of the pan-caspase inhibitor zVAD-FMK. Increased expression of the endoplasmic reticulum stress-associated proteins inositol-requiring 1α protein, C/EBP homologous protein, and binding immunoglobulin protein, and activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase, as well as decreased phosphorylation of Akt and reduced survivin expression were also observed in Piperine-treated HT-29 cells. Furthermore, Piperine inhibited colony formation by HT-29 cells, as well as the growth of HT-29 spheroids. Cell cycle arrest and endoplasmic reticulum stress-associated apoptosis following Piperine treatment of HT-29 cells provides the first evidence that Piperine may be useful in the treatment of colon cancer. © 2014 Wiley Periodicals, Inc.
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Piperine an alkaloid from black pepper inhibits growth of human colon cancer cells via g1 arrest and apoptosis triggered by endoplasmic reticulum stress
Molecular Carcinogenesis, 2015Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, Melanie Power R Coombs, David W HoskinAbstract:Piperine, a piperidine alkaloid present in black pepper, inhibits the growth of cancer cells, although the mechanism of action is not well understood. In this study, we show that Piperine (75-150 µM) inhibited the growth of several colon cancer cell lines but had little effect on the growth of normal fibroblasts and epithelial cells. Piperine inhibited HT-29 colon carcinoma cell proliferation by causing G1 phase cell cycle arrest that was associated with decreased expression of cyclins D1 and D3 and their activating partner cyclin-dependent kinases 4 and 6, as well as reduced phosphorylation of the retinoblastoma protein and up-regulation of p21/WAF1 and p27/KIP1 expression. In addition, Piperine caused hydroxyl radical production and apoptosis that was partially dependent on the production of reactive oxygen species. Piperine-treated HT-29 cells showed loss of mitochondrial membrane integrity and cleavage of poly (ADP-ribose) polymerase-1, as well as caspase activation and reduced apoptosis in the presence of the pan-caspase inhibitor zVAD-FMK. Increased expression of the endoplasmic reticulum stress-associated proteins inositol-requiring 1α protein, C/EBP homologous protein, and binding immunoglobulin protein, and activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase, as well as decreased phosphorylation of Akt and reduced survivin expression were also observed in Piperine-treated HT-29 cells. Furthermore, Piperine inhibited colony formation by HT-29 cells, as well as the growth of HT-29 spheroids. Cell cycle arrest and endoplasmic reticulum stress-associated apoptosis following Piperine treatment of HT-29 cells provides the first evidence that Piperine may be useful in the treatment of colon cancer.
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Piperine inhibits the growth and motility of triple negative breast cancer cells
Cancer Letters, 2015Co-Authors: Anna L Greenshields, Carolyn D Doucette, Kimberly M Sutton, Laurence Madera, Henry Annan, Paul B Yaffe, Allison Knickle, Zhongmin Dong, David W HoskinAbstract:Piperine, an alkaloid from black pepper, is reported to have anticancer activities. In this study, we investigated the effect of Piperine on the growth and motility of triple-negative breast cancer (TNBC) cells. Piperine inhibited the in vitro growth of TNBC cells, as well as hormone-dependent breast cancer cells, without affecting normal mammary epithelial cell growth. Exposure to Piperine decreased the percentage of TNBC cells in the G2 phase of the cell cycle. In addition, G1- and G2-associated protein expression was decreased and p21(Waf1/Cip1) expression was increased in Piperine-treated TNBC cells. Piperine also inhibited survival-promoting Akt activation in TNBC cells and caused caspase-dependent apoptosis via the mitochondrial pathway. Interestingly, combined treatment with Piperine and γ radiation was more cytotoxic for TNBC cells than γ radiation alone. The in vitro migration of Piperine-treated TNBC cells was impaired and expression of matrix metalloproteinase-2 and -9 mRNA was decreased, suggesting an antimetastatic effect by Piperine. Finally, intratumoral administration of Piperine inhibited the growth of TNBC xenografts in immune-deficient mice. Taken together, these findings suggest that Piperine may be useful in the treatment of TNBC.
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Piperine impairs cell cycle progression and causes reactive oxygen species dependent apoptosis in rectal cancer cells
Experimental and Molecular Pathology, 2013Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, David W HoskinAbstract:Piperine, an alkaloid phytochemical found in the fruit of black and long pepper plants, is reported to inhibit the growth of cancer cells; however, the mechanism of action in human cancer cells is not clear. In this study we investigated the effect of Piperine on the growth of HRT-18 human rectal adenocarcinoma cells. MTT assays showed that Piperine inhibited the metabolic activity of HRT-18 cells in a dose- and time-dependent fashion, suggesting a cytostatic and/or cytotoxic effect. Flow cytometric analysis of Oregon Green 488-stained and propidium iodide-stained HRT-18 cells showed that Piperine inhibited cell cycle progression. Piperine also caused HRT-18 cells to die by apoptosis, as determined by Annexin-V-FLUOS staining and characteristic changes in cell morphology. Flow cytometric analysis of dihydroethidium- and 2',7'-dichlorofluorescein diacetate-stained HRT-18 cells showed increased production of reactive oxygen species in Piperine-treated cells. Furthermore, the antioxidant N-acetylcysteine reduced apoptosis in cultures of Piperine-treated HRT-18 cells, indicating that Piperine-induced cytotoxicity was mediated at least in part by reactive oxygen species. The cytostatic and cytotoxic effects of Piperine on rectal cancer cells suggest that this dietary phytochemical may be useful in cancer treatment.
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Piperine a dietary phytochemical inhibits angiogenesis
Journal of Nutritional Biochemistry, 2013Co-Authors: Carolyn D Doucette, Ashley L Hilchie, Robert S Liwski, David W HoskinAbstract:Abstract Angiogenesis plays an important role in tumor progression. Piperine, a major alkaloid constituent of black pepper, has diverse physiological actions including killing of cancer cells; however, the effect of Piperine on angiogenesis is not known. Here we show that Piperine inhibited the proliferation and G 1 /S transition of human umbilical vein endothelial cells (HUVECs) without causing cell death. Piperine also inhibited HUVEC migration and tubule formation in vitro , as well as collagen-induced angiogenic activity by rat aorta explants and breast cancer cell-induced angiogenesis in chick embryos. Although Piperine binds to and activates the cation channel transient receptor potential vanilloid 1 (TRPV1), its effects on endothelial cells did not involve TRPV1 since the antiproliferative effect of Piperine was not affected by TRPV1-selective antagonists, nor did HUVECs express detectable TRPV1 mRNA. Importantly, Piperine inhibited phosphorylation of Ser 473 and Thr 308 residues of Akt (protein kinase B), which is a key regulator of endothelial cell function and angiogenesis. Consistent with Akt inhibition as the basis of Piperine's action on HUVECs, inhibition of the phosphoinositide-3 kinase/Akt signaling pathway with LY-294002 also inhibited HUVEC proliferation and collagen-induced angiogenesis. Taken together, these data support the further investigation of Piperine as an angiogenesis inhibitor for use in cancer treatment.
Paul B Yaffe - One of the best experts on this subject based on the ideXlab platform.
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Piperine an alkaloid from black pepper inhibits growth of human colon cancer cells via g1 arrest and apoptosis triggered by endoplasmic reticulum stress
Molecular Carcinogenesis, 2015Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, Melanie Power R Coombs, David W HoskinAbstract:Piperine, a piperidine alkaloid present in black pepper, inhibits the growth of cancer cells, although the mechanism of action is not well understood. In this study, we show that Piperine (75–150 µM) inhibited the growth of several colon cancer cell lines but had little effect on the growth of normal fibroblasts and epithelial cells. Piperine inhibited HT-29 colon carcinoma cell proliferation by causing G1 phase cell cycle arrest that was associated with decreased expression of cyclins D1 and D3 and their activating partner cyclin-dependent kinases 4 and 6, as well as reduced phosphorylation of the retinoblastoma protein and up-regulation of p21/WAF1 and p27/KIP1 expression. In addition, Piperine caused hydroxyl radical production and apoptosis that was partially dependent on the production of reactive oxygen species. Piperine-treated HT-29 cells showed loss of mitochondrial membrane integrity and cleavage of poly (ADP-ribose) polymerase-1, as well as caspase activation and reduced apoptosis in the presence of the pan-caspase inhibitor zVAD-FMK. Increased expression of the endoplasmic reticulum stress-associated proteins inositol-requiring 1α protein, C/EBP homologous protein, and binding immunoglobulin protein, and activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase, as well as decreased phosphorylation of Akt and reduced survivin expression were also observed in Piperine-treated HT-29 cells. Furthermore, Piperine inhibited colony formation by HT-29 cells, as well as the growth of HT-29 spheroids. Cell cycle arrest and endoplasmic reticulum stress-associated apoptosis following Piperine treatment of HT-29 cells provides the first evidence that Piperine may be useful in the treatment of colon cancer. © 2014 Wiley Periodicals, Inc.
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Piperine an alkaloid from black pepper inhibits growth of human colon cancer cells via g1 arrest and apoptosis triggered by endoplasmic reticulum stress
Molecular Carcinogenesis, 2015Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, Melanie Power R Coombs, David W HoskinAbstract:Piperine, a piperidine alkaloid present in black pepper, inhibits the growth of cancer cells, although the mechanism of action is not well understood. In this study, we show that Piperine (75-150 µM) inhibited the growth of several colon cancer cell lines but had little effect on the growth of normal fibroblasts and epithelial cells. Piperine inhibited HT-29 colon carcinoma cell proliferation by causing G1 phase cell cycle arrest that was associated with decreased expression of cyclins D1 and D3 and their activating partner cyclin-dependent kinases 4 and 6, as well as reduced phosphorylation of the retinoblastoma protein and up-regulation of p21/WAF1 and p27/KIP1 expression. In addition, Piperine caused hydroxyl radical production and apoptosis that was partially dependent on the production of reactive oxygen species. Piperine-treated HT-29 cells showed loss of mitochondrial membrane integrity and cleavage of poly (ADP-ribose) polymerase-1, as well as caspase activation and reduced apoptosis in the presence of the pan-caspase inhibitor zVAD-FMK. Increased expression of the endoplasmic reticulum stress-associated proteins inositol-requiring 1α protein, C/EBP homologous protein, and binding immunoglobulin protein, and activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase, as well as decreased phosphorylation of Akt and reduced survivin expression were also observed in Piperine-treated HT-29 cells. Furthermore, Piperine inhibited colony formation by HT-29 cells, as well as the growth of HT-29 spheroids. Cell cycle arrest and endoplasmic reticulum stress-associated apoptosis following Piperine treatment of HT-29 cells provides the first evidence that Piperine may be useful in the treatment of colon cancer.
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Piperine inhibits the growth and motility of triple negative breast cancer cells
Cancer Letters, 2015Co-Authors: Anna L Greenshields, Carolyn D Doucette, Kimberly M Sutton, Laurence Madera, Henry Annan, Paul B Yaffe, Allison Knickle, Zhongmin Dong, David W HoskinAbstract:Piperine, an alkaloid from black pepper, is reported to have anticancer activities. In this study, we investigated the effect of Piperine on the growth and motility of triple-negative breast cancer (TNBC) cells. Piperine inhibited the in vitro growth of TNBC cells, as well as hormone-dependent breast cancer cells, without affecting normal mammary epithelial cell growth. Exposure to Piperine decreased the percentage of TNBC cells in the G2 phase of the cell cycle. In addition, G1- and G2-associated protein expression was decreased and p21(Waf1/Cip1) expression was increased in Piperine-treated TNBC cells. Piperine also inhibited survival-promoting Akt activation in TNBC cells and caused caspase-dependent apoptosis via the mitochondrial pathway. Interestingly, combined treatment with Piperine and γ radiation was more cytotoxic for TNBC cells than γ radiation alone. The in vitro migration of Piperine-treated TNBC cells was impaired and expression of matrix metalloproteinase-2 and -9 mRNA was decreased, suggesting an antimetastatic effect by Piperine. Finally, intratumoral administration of Piperine inhibited the growth of TNBC xenografts in immune-deficient mice. Taken together, these findings suggest that Piperine may be useful in the treatment of TNBC.
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Piperine impairs cell cycle progression and causes reactive oxygen species dependent apoptosis in rectal cancer cells
Experimental and Molecular Pathology, 2013Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, David W HoskinAbstract:Piperine, an alkaloid phytochemical found in the fruit of black and long pepper plants, is reported to inhibit the growth of cancer cells; however, the mechanism of action in human cancer cells is not clear. In this study we investigated the effect of Piperine on the growth of HRT-18 human rectal adenocarcinoma cells. MTT assays showed that Piperine inhibited the metabolic activity of HRT-18 cells in a dose- and time-dependent fashion, suggesting a cytostatic and/or cytotoxic effect. Flow cytometric analysis of Oregon Green 488-stained and propidium iodide-stained HRT-18 cells showed that Piperine inhibited cell cycle progression. Piperine also caused HRT-18 cells to die by apoptosis, as determined by Annexin-V-FLUOS staining and characteristic changes in cell morphology. Flow cytometric analysis of dihydroethidium- and 2',7'-dichlorofluorescein diacetate-stained HRT-18 cells showed increased production of reactive oxygen species in Piperine-treated cells. Furthermore, the antioxidant N-acetylcysteine reduced apoptosis in cultures of Piperine-treated HRT-18 cells, indicating that Piperine-induced cytotoxicity was mediated at least in part by reactive oxygen species. The cytostatic and cytotoxic effects of Piperine on rectal cancer cells suggest that this dietary phytochemical may be useful in cancer treatment.
Carolyn D Doucette - One of the best experts on this subject based on the ideXlab platform.
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Piperine an alkaloid from black pepper inhibits growth of human colon cancer cells via g1 arrest and apoptosis triggered by endoplasmic reticulum stress
Molecular Carcinogenesis, 2015Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, Melanie Power R Coombs, David W HoskinAbstract:Piperine, a piperidine alkaloid present in black pepper, inhibits the growth of cancer cells, although the mechanism of action is not well understood. In this study, we show that Piperine (75–150 µM) inhibited the growth of several colon cancer cell lines but had little effect on the growth of normal fibroblasts and epithelial cells. Piperine inhibited HT-29 colon carcinoma cell proliferation by causing G1 phase cell cycle arrest that was associated with decreased expression of cyclins D1 and D3 and their activating partner cyclin-dependent kinases 4 and 6, as well as reduced phosphorylation of the retinoblastoma protein and up-regulation of p21/WAF1 and p27/KIP1 expression. In addition, Piperine caused hydroxyl radical production and apoptosis that was partially dependent on the production of reactive oxygen species. Piperine-treated HT-29 cells showed loss of mitochondrial membrane integrity and cleavage of poly (ADP-ribose) polymerase-1, as well as caspase activation and reduced apoptosis in the presence of the pan-caspase inhibitor zVAD-FMK. Increased expression of the endoplasmic reticulum stress-associated proteins inositol-requiring 1α protein, C/EBP homologous protein, and binding immunoglobulin protein, and activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase, as well as decreased phosphorylation of Akt and reduced survivin expression were also observed in Piperine-treated HT-29 cells. Furthermore, Piperine inhibited colony formation by HT-29 cells, as well as the growth of HT-29 spheroids. Cell cycle arrest and endoplasmic reticulum stress-associated apoptosis following Piperine treatment of HT-29 cells provides the first evidence that Piperine may be useful in the treatment of colon cancer. © 2014 Wiley Periodicals, Inc.
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Piperine an alkaloid from black pepper inhibits growth of human colon cancer cells via g1 arrest and apoptosis triggered by endoplasmic reticulum stress
Molecular Carcinogenesis, 2015Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, Melanie Power R Coombs, David W HoskinAbstract:Piperine, a piperidine alkaloid present in black pepper, inhibits the growth of cancer cells, although the mechanism of action is not well understood. In this study, we show that Piperine (75-150 µM) inhibited the growth of several colon cancer cell lines but had little effect on the growth of normal fibroblasts and epithelial cells. Piperine inhibited HT-29 colon carcinoma cell proliferation by causing G1 phase cell cycle arrest that was associated with decreased expression of cyclins D1 and D3 and their activating partner cyclin-dependent kinases 4 and 6, as well as reduced phosphorylation of the retinoblastoma protein and up-regulation of p21/WAF1 and p27/KIP1 expression. In addition, Piperine caused hydroxyl radical production and apoptosis that was partially dependent on the production of reactive oxygen species. Piperine-treated HT-29 cells showed loss of mitochondrial membrane integrity and cleavage of poly (ADP-ribose) polymerase-1, as well as caspase activation and reduced apoptosis in the presence of the pan-caspase inhibitor zVAD-FMK. Increased expression of the endoplasmic reticulum stress-associated proteins inositol-requiring 1α protein, C/EBP homologous protein, and binding immunoglobulin protein, and activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase, as well as decreased phosphorylation of Akt and reduced survivin expression were also observed in Piperine-treated HT-29 cells. Furthermore, Piperine inhibited colony formation by HT-29 cells, as well as the growth of HT-29 spheroids. Cell cycle arrest and endoplasmic reticulum stress-associated apoptosis following Piperine treatment of HT-29 cells provides the first evidence that Piperine may be useful in the treatment of colon cancer.
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Piperine inhibits the growth and motility of triple negative breast cancer cells
Cancer Letters, 2015Co-Authors: Anna L Greenshields, Carolyn D Doucette, Kimberly M Sutton, Laurence Madera, Henry Annan, Paul B Yaffe, Allison Knickle, Zhongmin Dong, David W HoskinAbstract:Piperine, an alkaloid from black pepper, is reported to have anticancer activities. In this study, we investigated the effect of Piperine on the growth and motility of triple-negative breast cancer (TNBC) cells. Piperine inhibited the in vitro growth of TNBC cells, as well as hormone-dependent breast cancer cells, without affecting normal mammary epithelial cell growth. Exposure to Piperine decreased the percentage of TNBC cells in the G2 phase of the cell cycle. In addition, G1- and G2-associated protein expression was decreased and p21(Waf1/Cip1) expression was increased in Piperine-treated TNBC cells. Piperine also inhibited survival-promoting Akt activation in TNBC cells and caused caspase-dependent apoptosis via the mitochondrial pathway. Interestingly, combined treatment with Piperine and γ radiation was more cytotoxic for TNBC cells than γ radiation alone. The in vitro migration of Piperine-treated TNBC cells was impaired and expression of matrix metalloproteinase-2 and -9 mRNA was decreased, suggesting an antimetastatic effect by Piperine. Finally, intratumoral administration of Piperine inhibited the growth of TNBC xenografts in immune-deficient mice. Taken together, these findings suggest that Piperine may be useful in the treatment of TNBC.
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Piperine impairs cell cycle progression and causes reactive oxygen species dependent apoptosis in rectal cancer cells
Experimental and Molecular Pathology, 2013Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, David W HoskinAbstract:Piperine, an alkaloid phytochemical found in the fruit of black and long pepper plants, is reported to inhibit the growth of cancer cells; however, the mechanism of action in human cancer cells is not clear. In this study we investigated the effect of Piperine on the growth of HRT-18 human rectal adenocarcinoma cells. MTT assays showed that Piperine inhibited the metabolic activity of HRT-18 cells in a dose- and time-dependent fashion, suggesting a cytostatic and/or cytotoxic effect. Flow cytometric analysis of Oregon Green 488-stained and propidium iodide-stained HRT-18 cells showed that Piperine inhibited cell cycle progression. Piperine also caused HRT-18 cells to die by apoptosis, as determined by Annexin-V-FLUOS staining and characteristic changes in cell morphology. Flow cytometric analysis of dihydroethidium- and 2',7'-dichlorofluorescein diacetate-stained HRT-18 cells showed increased production of reactive oxygen species in Piperine-treated cells. Furthermore, the antioxidant N-acetylcysteine reduced apoptosis in cultures of Piperine-treated HRT-18 cells, indicating that Piperine-induced cytotoxicity was mediated at least in part by reactive oxygen species. The cytostatic and cytotoxic effects of Piperine on rectal cancer cells suggest that this dietary phytochemical may be useful in cancer treatment.
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Piperine a dietary phytochemical inhibits angiogenesis
Journal of Nutritional Biochemistry, 2013Co-Authors: Carolyn D Doucette, Ashley L Hilchie, Robert S Liwski, David W HoskinAbstract:Abstract Angiogenesis plays an important role in tumor progression. Piperine, a major alkaloid constituent of black pepper, has diverse physiological actions including killing of cancer cells; however, the effect of Piperine on angiogenesis is not known. Here we show that Piperine inhibited the proliferation and G 1 /S transition of human umbilical vein endothelial cells (HUVECs) without causing cell death. Piperine also inhibited HUVEC migration and tubule formation in vitro , as well as collagen-induced angiogenic activity by rat aorta explants and breast cancer cell-induced angiogenesis in chick embryos. Although Piperine binds to and activates the cation channel transient receptor potential vanilloid 1 (TRPV1), its effects on endothelial cells did not involve TRPV1 since the antiproliferative effect of Piperine was not affected by TRPV1-selective antagonists, nor did HUVECs express detectable TRPV1 mRNA. Importantly, Piperine inhibited phosphorylation of Ser 473 and Thr 308 residues of Akt (protein kinase B), which is a key regulator of endothelial cell function and angiogenesis. Consistent with Akt inhibition as the basis of Piperine's action on HUVECs, inhibition of the phosphoinositide-3 kinase/Akt signaling pathway with LY-294002 also inhibited HUVEC proliferation and collagen-induced angiogenesis. Taken together, these data support the further investigation of Piperine as an angiogenesis inhibitor for use in cancer treatment.
G Kuttan - One of the best experts on this subject based on the ideXlab platform.
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Piperine is a potent inhibitor of nuclear factor κb nf κb c fos creb atf 2 and proinflammatory cytokine gene expression in b16f 10 melanoma cells
International Immunopharmacology, 2004Co-Authors: C R Pradeep, G KuttanAbstract:Immune regulation, induction of various inflammatory and growth regulatory genes such as IL-1beta, IL-6, TNF-alpha and GM-CSF require activation of transcription factors such as nuclear factor-kappaB (NF-kappaB), activated transcription factor (ATF-2), c-Fos and cAMP response element-binding protein (CREB). Untreated B16F-10 cells produce very high amount of proinflammatory cytokines such as IL-1beta, IL-6, TNF-alpha and GM-CSF. Piperine treatment significantly reduced the above proinflammatory cytokines. We also found that Piperine could reduce the expression of IL-1beta, IL-6, TNF-alpha, GM-CSF and IL-12p40 genes. Piperine at a concentration of 2.5, 5 and 10 microg/ml inhibited the collagen matrix invasion of B16F-10 melanoma cells in a dose-dependent manner. Piperine could inhibit the matrix metalloproteinase production which was demonstrated by zymographic analysis. We found that the nuclear translocation of p65, p50, c-Rel subunits of NF-kappaB and other transcription factors such as ATF-2, c-Fos and CREB were inhibited by the treatment of Piperine.
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effect of Piperine on the inhibition of lung metastasis induced b16f 10 melanoma cells in mice
Clinical & Experimental Metastasis, 2002Co-Authors: C R Pradeep, G KuttanAbstract:The effect of Piperine on the inhibition of lung metastasis induced by B16F-10 melanoma cells was studied in C57BL/6 mice. Simultaneous administration of the compound with tumor induction produced a significant reduction (95.2%) in tumor nodule formation. Increased lung collagen hydroxyproline (22.37 microg/mg protein) in the metastasized lungs of the control animals compared to normal animals (0.95 microg/mg protein) was significantly reduced (2.59 microg/mg protein) in the Piperine-treated animals. The high amount of uronic acid (355.83 microg/100 mg tissue) in the metastasized control animals was significantly reduced (65 microg/100 mg tissue) in the animals treated with Piperine. Lung hexosamine content was also significantly reduced in the Piperine-treated animals (0.98 mg/100 mg lyophilized tissue) compared to the untreated tumor-bearing animals (4.2 mg/100 mg lyophilized tissue). The elevated levels of serum sialic acid and serum gamma glutamyl transpeptidase activity in the untreated control animals was significantly reduced in the animals treated with Piperine. The Piperine-treated animals even survived the experiment (90 days). Histopathology of the lung tissue also correlated with the lifespan of the drug-treated animals. Our results demonstrate the antimetastatic activity of Piperine, an alkaloid present in plants such as Piper nigrum and Piper longum.
Mark Walsh - One of the best experts on this subject based on the ideXlab platform.
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Piperine an alkaloid from black pepper inhibits growth of human colon cancer cells via g1 arrest and apoptosis triggered by endoplasmic reticulum stress
Molecular Carcinogenesis, 2015Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, Melanie Power R Coombs, David W HoskinAbstract:Piperine, a piperidine alkaloid present in black pepper, inhibits the growth of cancer cells, although the mechanism of action is not well understood. In this study, we show that Piperine (75-150 µM) inhibited the growth of several colon cancer cell lines but had little effect on the growth of normal fibroblasts and epithelial cells. Piperine inhibited HT-29 colon carcinoma cell proliferation by causing G1 phase cell cycle arrest that was associated with decreased expression of cyclins D1 and D3 and their activating partner cyclin-dependent kinases 4 and 6, as well as reduced phosphorylation of the retinoblastoma protein and up-regulation of p21/WAF1 and p27/KIP1 expression. In addition, Piperine caused hydroxyl radical production and apoptosis that was partially dependent on the production of reactive oxygen species. Piperine-treated HT-29 cells showed loss of mitochondrial membrane integrity and cleavage of poly (ADP-ribose) polymerase-1, as well as caspase activation and reduced apoptosis in the presence of the pan-caspase inhibitor zVAD-FMK. Increased expression of the endoplasmic reticulum stress-associated proteins inositol-requiring 1α protein, C/EBP homologous protein, and binding immunoglobulin protein, and activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase, as well as decreased phosphorylation of Akt and reduced survivin expression were also observed in Piperine-treated HT-29 cells. Furthermore, Piperine inhibited colony formation by HT-29 cells, as well as the growth of HT-29 spheroids. Cell cycle arrest and endoplasmic reticulum stress-associated apoptosis following Piperine treatment of HT-29 cells provides the first evidence that Piperine may be useful in the treatment of colon cancer.
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Piperine an alkaloid from black pepper inhibits growth of human colon cancer cells via g1 arrest and apoptosis triggered by endoplasmic reticulum stress
Molecular Carcinogenesis, 2015Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, Melanie Power R Coombs, David W HoskinAbstract:Piperine, a piperidine alkaloid present in black pepper, inhibits the growth of cancer cells, although the mechanism of action is not well understood. In this study, we show that Piperine (75–150 µM) inhibited the growth of several colon cancer cell lines but had little effect on the growth of normal fibroblasts and epithelial cells. Piperine inhibited HT-29 colon carcinoma cell proliferation by causing G1 phase cell cycle arrest that was associated with decreased expression of cyclins D1 and D3 and their activating partner cyclin-dependent kinases 4 and 6, as well as reduced phosphorylation of the retinoblastoma protein and up-regulation of p21/WAF1 and p27/KIP1 expression. In addition, Piperine caused hydroxyl radical production and apoptosis that was partially dependent on the production of reactive oxygen species. Piperine-treated HT-29 cells showed loss of mitochondrial membrane integrity and cleavage of poly (ADP-ribose) polymerase-1, as well as caspase activation and reduced apoptosis in the presence of the pan-caspase inhibitor zVAD-FMK. Increased expression of the endoplasmic reticulum stress-associated proteins inositol-requiring 1α protein, C/EBP homologous protein, and binding immunoglobulin protein, and activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase, as well as decreased phosphorylation of Akt and reduced survivin expression were also observed in Piperine-treated HT-29 cells. Furthermore, Piperine inhibited colony formation by HT-29 cells, as well as the growth of HT-29 spheroids. Cell cycle arrest and endoplasmic reticulum stress-associated apoptosis following Piperine treatment of HT-29 cells provides the first evidence that Piperine may be useful in the treatment of colon cancer. © 2014 Wiley Periodicals, Inc.
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Piperine impairs cell cycle progression and causes reactive oxygen species dependent apoptosis in rectal cancer cells
Experimental and Molecular Pathology, 2013Co-Authors: Paul B Yaffe, Carolyn D Doucette, Mark Walsh, David W HoskinAbstract:Piperine, an alkaloid phytochemical found in the fruit of black and long pepper plants, is reported to inhibit the growth of cancer cells; however, the mechanism of action in human cancer cells is not clear. In this study we investigated the effect of Piperine on the growth of HRT-18 human rectal adenocarcinoma cells. MTT assays showed that Piperine inhibited the metabolic activity of HRT-18 cells in a dose- and time-dependent fashion, suggesting a cytostatic and/or cytotoxic effect. Flow cytometric analysis of Oregon Green 488-stained and propidium iodide-stained HRT-18 cells showed that Piperine inhibited cell cycle progression. Piperine also caused HRT-18 cells to die by apoptosis, as determined by Annexin-V-FLUOS staining and characteristic changes in cell morphology. Flow cytometric analysis of dihydroethidium- and 2',7'-dichlorofluorescein diacetate-stained HRT-18 cells showed increased production of reactive oxygen species in Piperine-treated cells. Furthermore, the antioxidant N-acetylcysteine reduced apoptosis in cultures of Piperine-treated HRT-18 cells, indicating that Piperine-induced cytotoxicity was mediated at least in part by reactive oxygen species. The cytostatic and cytotoxic effects of Piperine on rectal cancer cells suggest that this dietary phytochemical may be useful in cancer treatment.