The Experts below are selected from a list of 330 Experts worldwide ranked by ideXlab platform
Aiyun Wang - One of the best experts on this subject based on the ideXlab platform.
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Beta Elemene inhibits breast cancer metastasis through blocking pyruvate kinase m2 dimerization and nuclear translocation
Journal of Cellular and Molecular Medicine, 2019Co-Authors: Yanhong Pan, Wei Wang, Shuai Huang, Zhonghong Wei, Yuzhu Cao, Qi Jia, Chuan Chai, Qian Zheng, Lei Zhang, Aiyun WangAbstract:Pyruvate kinase M2 (PKM2), playing a central role in regulating aerobic glycolysis, was considered as a promising target for cancer therapy. However, its role in cancer metastasis is rarely known. Here, we found a tight relationship between PKM2 and breast cancer metastasis, demonstrated by the findings that Beta-Elemene (β-Elemene), an approved drug for complementary cancer therapy, exerted distinct anti-metastatic activity dependent on PKM2. The results indicated that β-Elemene inhibited breast cancer cell migration, invasion in vitro as well as metastases in vivo. β-Elemene further inhibited the process of aerobic glycolysis and decreased the utilization of glucose and the production of pyruvate and lactate through suppressing pyruvate kinase activity by modulating the transformation of dimeric and tetrameric forms of PKM2. Further analysis revealed that β-Elemene suppressed aerobic glycolysis by blocking PKM2 nuclear translocation and the expression of EGFR, GLUT1 and LDHA by influencing the expression of importin α5. Furthermore, the effect of β-Elemene on migration, invasion, PKM2 transformation, and nuclear translocation could be reversed in part by fructose-1,6-bisphosphate (FBP) and L-cysteine. Taken together, tetrameric transformation and nuclear translocation of PKM2 are essential for cancer metastasis, and β-Elemene inhibited breast cancer metastasis via blocking aerobic glycolysis mediated by dimeric PKM2 transformation and nuclear translocation, being a promising anti-metastatic agent from natural compounds.
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Beta Elemene inhibits melanoma growth and metastasis via suppressing vascular endothelial growth factor mediated angiogenesis
Cancer Chemotherapy and Pharmacology, 2011Co-Authors: Wenxing Chen, Ming Gao, Aiyun WangAbstract:It was to assess antiangiogenic effect of β-Elemene in vitro and in vivo, and it was involved in inhibiting melanoma growth and metastasis, as well as to elucidate its intrinsic mechanism. Inhibitive effect of β-Elemene on B16F10 cells was performed by cell proliferation assay. Angiogenesis assays in vitro including rat aortic ring and chick embryo chorioallantoic membrane were used, as well as melanoma growth and metastasis assay in C57BL/6 mice. Vascular endothelial growth factor (VEGF) expression in vitro and in vivo was measured respectively by western blot analysis and enzyme-linked immunosorbent assay (ELISA). Immunohistochemistry analysis of CD34 and VEGF expression in primary melanoma was also presented. β-Elemene inhibited B16BF10 cell proliferation starting from 200 μM, but VEGF from 20 μM. Both 20 and 50 μM β-Elemene in vitro inhibited VEGF-induced sprouting vessel of rat aortic ring and microvessel formation of chick embryo chorioallantoic membrane. In vivo, tumor size of primary melanoma in mice intraperitoneally treated with β-Elemene was significantly smaller than that of the control; CD34 expression of primary melanoma was also suppressed; and the metastatic melanoma colonies and content of melanin in lung were detected obviously decreased in mice of β-Elemene-treated groups. Furthermore, results of VEGF expressing in primary melanoma, serum and lung of mice also disclosed that VEGF was inhibited in vivo. β-Elemene inhibited melanoma growth and metastasis through suppressing VEGF-mediated angiogenesis. It is a natural potential antiangiogenic agent.
Wenxing Chen - One of the best experts on this subject based on the ideXlab platform.
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blocking dimeric pyruvate kinase m2 transformation and nuclear translocation leading to suppression of aerobic glycolysis mediates Beta Elemene inhibition of breast cancer metastasis
Social Science Research Network, 2018Co-Authors: Wenxing Chen, Yanhong Pan, Wei Wang, Shuai Huang, Zhonghong Wei, Yuzhu Cao, Qi Jia, Chuan Chai, Qian Zheng, Lei ZhangAbstract:Pyruvate kinase M2 (PKM2) plays a central role in regulating aerobic glycolysis and is considered as a potential target for cancer therapy. However, its role in cancer metastasis is rarely known. Here, we found a tight relationship between PKM2 and breast cancer metastasis, which is demonstrated by the finding that Beta-Elemene (β-Elemene), an approved drug for complementary cancer therapy, exerted distinct anti-metastatic activity dependent on PKM2. The results indicated thatβ-Elemene inhibited breast cancer cell migration, invasion and angiogenesis. β-Elemene also inhibited the process of glycolysis, and decreased the utilization of glucose and the production of pyruvate and lactate through suppressing pyruvate kinase activity by modulating the transformation of dimeric and tetrameric forms of PKM2, which was reversed in part by fructose-1,6-bisphosphate (FBP) or L-cysteine. Our further analysis revealed that β-Elemene suppressed aerobic glycolysis through inhibiting the nuclear transportation of PKM2 and the expression of GLUT1, MCT1, MCT4 and LDHA by influencing the expression of importin α5. Additionally, β-Elemene remarkably inhibited the breast cancer metastases in lung and liver and selectively influenced the glycolysis of the lung and liver metastatic foci in mouse models. Taken together, tetrameric transformation and nuclear translocation of PKM2 are essential for cancer metastasis, and β-Elemene inhibits breast cancer metastasis via blocking aerobic glycolysis induced by dimeric PKM2 transformation and EGFR-importin α5 mediated PKM2 nuclear translocation, being a promising anti-metastatic agent. Funding Statement: The work was supported by National Natural Science Foundation of China (No. 81673648, 81673725, 81573859, 81603339), Natural Science Foundation of Higher School of Jiangsu Province (17KJA360003), and the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD). Declaration of Interests: The authors declare that they have no conflict of interest. Ethics Approval Statement: All animal studies were approved by the Animal Care and Use Committee of Nanjing University of Chinese Medicine. All mouse experimental procedures were performed in accordance with the Regulations for the Administration of Affairs Concerning Experimental Animals approved by the State Council of People’s Republic of China.
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Beta Elemene inhibits melanoma growth and metastasis via suppressing vascular endothelial growth factor mediated angiogenesis
Cancer Chemotherapy and Pharmacology, 2011Co-Authors: Wenxing Chen, Ming Gao, Aiyun WangAbstract:It was to assess antiangiogenic effect of β-Elemene in vitro and in vivo, and it was involved in inhibiting melanoma growth and metastasis, as well as to elucidate its intrinsic mechanism. Inhibitive effect of β-Elemene on B16F10 cells was performed by cell proliferation assay. Angiogenesis assays in vitro including rat aortic ring and chick embryo chorioallantoic membrane were used, as well as melanoma growth and metastasis assay in C57BL/6 mice. Vascular endothelial growth factor (VEGF) expression in vitro and in vivo was measured respectively by western blot analysis and enzyme-linked immunosorbent assay (ELISA). Immunohistochemistry analysis of CD34 and VEGF expression in primary melanoma was also presented. β-Elemene inhibited B16BF10 cell proliferation starting from 200 μM, but VEGF from 20 μM. Both 20 and 50 μM β-Elemene in vitro inhibited VEGF-induced sprouting vessel of rat aortic ring and microvessel formation of chick embryo chorioallantoic membrane. In vivo, tumor size of primary melanoma in mice intraperitoneally treated with β-Elemene was significantly smaller than that of the control; CD34 expression of primary melanoma was also suppressed; and the metastatic melanoma colonies and content of melanin in lung were detected obviously decreased in mice of β-Elemene-treated groups. Furthermore, results of VEGF expressing in primary melanoma, serum and lung of mice also disclosed that VEGF was inhibited in vivo. β-Elemene inhibited melanoma growth and metastasis through suppressing VEGF-mediated angiogenesis. It is a natural potential antiangiogenic agent.
Moreno P. R. H. - One of the best experts on this subject based on the ideXlab platform.
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Chemical Composition and Antimicrobial Activity of the Essential Oil from Rollinia sericea (REFr.) REFr. (Annonaceae) Leaves
ALLURED PUBL CORP, 2010Co-Authors: Ito R. K., Lima M. E. L., Moreno P. R. H.Abstract:The chemical composition of the essential oil of Rollinia sericea (R.E.Fr.) R.E.Fr. leaves was determined by GC and GC/MS analysis. The analysis revealed the presence mainly of sesquiterpenes: Beta-Elemene (10%), Beta-caryophyllene (10.0%), bicyclogermacrene (9.1%), germacrene-D (8.2%), bicycloElemene (6.2%) and (Z)-nerolidol (5.3%). Rollinia sericea oil was able to inhibit the growth of both fungi Aspergillus niger (16404) and Candida albicans (ATCC 10231) as well as the Gram-positive bacterium Staphyloccocus aureus (ATCC 6538) but it was inactive against the Gram-negative bacteria Escherichia coli (ATCC 8739) and Pseudomonas aeruginosa (ATCC 9027)
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Chemical Composition and Antimicrobial Activity of the Essential Oil from Rollinia sericea (REFr.) REFr. (Annonaceae) Leaves
ALLURED PUBL CORP, 2010Co-Authors: Ito R. K., Lima M. E. L., Moreno P. R. H.Abstract:The chemical composition of the essential oil of Rollinia sericea (R.E.Fr.) R.E.Fr. leaves was determined by GC and GC/MS analysis. The analysis revealed the presence mainly of sesquiterpenes: Beta-Elemene (10%), Beta-caryophyllene (10.0%), bicyclogermacrene (9.1%), germacrene-D (8.2%), bicycloElemene (6.2%) and (Z)-nerolidol (5.3%). Rollinia sericea oil was able to inhibit the growth of both fungi Aspergillus niger (16404) and Candida albicans (ATCC 10231) as well as the Gram-positive bacterium Staphyloccocus aureus (ATCC 6538) but it was inactive against the Gram-negative bacteria Escherichia coli (ATCC 8739) and Pseudomonas aeruginosa (ATCC 9027).Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)BIOTA/FAPESPConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)CNP
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Chemical Composition and Antimicrobial Activity of the Essential Oil from Croton heterocalyx Baill. (Euphorbiaceae s.s.) Leaves
ALLURED PUBL CORP, 2009Co-Authors: Moreno P. R. H., Lima, Marcos Enoque Leite, Caruzo, Maria Beatriz Rossi, Torres, Daniela Santos Carneiro, Cordeiro Ines, Young, Maria Claudia MarxAbstract:The chemical composition and the antimicrobial activity of the essential oil from Croton heterocalyx leaves were evaluated. The oil which was analyzed by GC and GUMS was found to contain germacrene D (12.5%), bicyclogermacrene (11.2%), delta-Elemene (9.2%) Beta-Elemene (8.2%), spathulenol (6.9%), linalool (5.4%) and 1,8-cineole (3.7%) its major components. Croton. heterocalyx oil displayed a high inhibitory activity against the fungi Aspergillus niger (16404) and Candida albicans (ATCC 10231.) as well its the Gram-positive bacterium Staphylococcus aureus (ATCC 6538), hut a very weak activity was observed for the Gram-negative bacteria Escherichia coli (ATCC 8739) and Pseudomonas aeruginosa (ATCC 9027)
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Chemical Composition and Antimicrobial Activity of the Essential Oil from Croton heterocalyx Baill. (Euphorbiaceae s.s.) Leaves
ALLURED PUBL CORP, 2009Co-Authors: Moreno P. R. H., Lima, Marcos Enoque Leite, Caruzo, Maria Beatriz Rossi, Torres, Daniela Santos Carneiro, Cordeiro Ines, Young, Maria Claudia MarxAbstract:The chemical composition and the antimicrobial activity of the essential oil from Croton heterocalyx leaves were evaluated. The oil which was analyzed by GC and GUMS was found to contain germacrene D (12.5%), bicyclogermacrene (11.2%), delta-Elemene (9.2%) Beta-Elemene (8.2%), spathulenol (6.9%), linalool (5.4%) and 1,8-cineole (3.7%) its major components. Croton. heterocalyx oil displayed a high inhibitory activity against the fungi Aspergillus niger (16404) and Candida albicans (ATCC 10231.) as well its the Gram-positive bacterium Staphylococcus aureus (ATCC 6538), hut a very weak activity was observed for the Gram-negative bacteria Escherichia coli (ATCC 8739) and Pseudomonas aeruginosa (ATCC 9027).BIOTA/FAPESP ProgramFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)CNPqConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq
Lei Zhang - One of the best experts on this subject based on the ideXlab platform.
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Beta Elemene inhibits breast cancer metastasis through blocking pyruvate kinase m2 dimerization and nuclear translocation
Journal of Cellular and Molecular Medicine, 2019Co-Authors: Yanhong Pan, Wei Wang, Shuai Huang, Zhonghong Wei, Yuzhu Cao, Qi Jia, Chuan Chai, Qian Zheng, Lei Zhang, Aiyun WangAbstract:Pyruvate kinase M2 (PKM2), playing a central role in regulating aerobic glycolysis, was considered as a promising target for cancer therapy. However, its role in cancer metastasis is rarely known. Here, we found a tight relationship between PKM2 and breast cancer metastasis, demonstrated by the findings that Beta-Elemene (β-Elemene), an approved drug for complementary cancer therapy, exerted distinct anti-metastatic activity dependent on PKM2. The results indicated that β-Elemene inhibited breast cancer cell migration, invasion in vitro as well as metastases in vivo. β-Elemene further inhibited the process of aerobic glycolysis and decreased the utilization of glucose and the production of pyruvate and lactate through suppressing pyruvate kinase activity by modulating the transformation of dimeric and tetrameric forms of PKM2. Further analysis revealed that β-Elemene suppressed aerobic glycolysis by blocking PKM2 nuclear translocation and the expression of EGFR, GLUT1 and LDHA by influencing the expression of importin α5. Furthermore, the effect of β-Elemene on migration, invasion, PKM2 transformation, and nuclear translocation could be reversed in part by fructose-1,6-bisphosphate (FBP) and L-cysteine. Taken together, tetrameric transformation and nuclear translocation of PKM2 are essential for cancer metastasis, and β-Elemene inhibited breast cancer metastasis via blocking aerobic glycolysis mediated by dimeric PKM2 transformation and nuclear translocation, being a promising anti-metastatic agent from natural compounds.
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blocking dimeric pyruvate kinase m2 transformation and nuclear translocation leading to suppression of aerobic glycolysis mediates Beta Elemene inhibition of breast cancer metastasis
Social Science Research Network, 2018Co-Authors: Wenxing Chen, Yanhong Pan, Wei Wang, Shuai Huang, Zhonghong Wei, Yuzhu Cao, Qi Jia, Chuan Chai, Qian Zheng, Lei ZhangAbstract:Pyruvate kinase M2 (PKM2) plays a central role in regulating aerobic glycolysis and is considered as a potential target for cancer therapy. However, its role in cancer metastasis is rarely known. Here, we found a tight relationship between PKM2 and breast cancer metastasis, which is demonstrated by the finding that Beta-Elemene (β-Elemene), an approved drug for complementary cancer therapy, exerted distinct anti-metastatic activity dependent on PKM2. The results indicated thatβ-Elemene inhibited breast cancer cell migration, invasion and angiogenesis. β-Elemene also inhibited the process of glycolysis, and decreased the utilization of glucose and the production of pyruvate and lactate through suppressing pyruvate kinase activity by modulating the transformation of dimeric and tetrameric forms of PKM2, which was reversed in part by fructose-1,6-bisphosphate (FBP) or L-cysteine. Our further analysis revealed that β-Elemene suppressed aerobic glycolysis through inhibiting the nuclear transportation of PKM2 and the expression of GLUT1, MCT1, MCT4 and LDHA by influencing the expression of importin α5. Additionally, β-Elemene remarkably inhibited the breast cancer metastases in lung and liver and selectively influenced the glycolysis of the lung and liver metastatic foci in mouse models. Taken together, tetrameric transformation and nuclear translocation of PKM2 are essential for cancer metastasis, and β-Elemene inhibits breast cancer metastasis via blocking aerobic glycolysis induced by dimeric PKM2 transformation and EGFR-importin α5 mediated PKM2 nuclear translocation, being a promising anti-metastatic agent. Funding Statement: The work was supported by National Natural Science Foundation of China (No. 81673648, 81673725, 81573859, 81603339), Natural Science Foundation of Higher School of Jiangsu Province (17KJA360003), and the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD). Declaration of Interests: The authors declare that they have no conflict of interest. Ethics Approval Statement: All animal studies were approved by the Animal Care and Use Committee of Nanjing University of Chinese Medicine. All mouse experimental procedures were performed in accordance with the Regulations for the Administration of Affairs Concerning Experimental Animals approved by the State Council of People’s Republic of China.
Yanhong Pan - One of the best experts on this subject based on the ideXlab platform.
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Beta Elemene inhibits breast cancer metastasis through blocking pyruvate kinase m2 dimerization and nuclear translocation
Journal of Cellular and Molecular Medicine, 2019Co-Authors: Yanhong Pan, Wei Wang, Shuai Huang, Zhonghong Wei, Yuzhu Cao, Qi Jia, Chuan Chai, Qian Zheng, Lei Zhang, Aiyun WangAbstract:Pyruvate kinase M2 (PKM2), playing a central role in regulating aerobic glycolysis, was considered as a promising target for cancer therapy. However, its role in cancer metastasis is rarely known. Here, we found a tight relationship between PKM2 and breast cancer metastasis, demonstrated by the findings that Beta-Elemene (β-Elemene), an approved drug for complementary cancer therapy, exerted distinct anti-metastatic activity dependent on PKM2. The results indicated that β-Elemene inhibited breast cancer cell migration, invasion in vitro as well as metastases in vivo. β-Elemene further inhibited the process of aerobic glycolysis and decreased the utilization of glucose and the production of pyruvate and lactate through suppressing pyruvate kinase activity by modulating the transformation of dimeric and tetrameric forms of PKM2. Further analysis revealed that β-Elemene suppressed aerobic glycolysis by blocking PKM2 nuclear translocation and the expression of EGFR, GLUT1 and LDHA by influencing the expression of importin α5. Furthermore, the effect of β-Elemene on migration, invasion, PKM2 transformation, and nuclear translocation could be reversed in part by fructose-1,6-bisphosphate (FBP) and L-cysteine. Taken together, tetrameric transformation and nuclear translocation of PKM2 are essential for cancer metastasis, and β-Elemene inhibited breast cancer metastasis via blocking aerobic glycolysis mediated by dimeric PKM2 transformation and nuclear translocation, being a promising anti-metastatic agent from natural compounds.
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blocking dimeric pyruvate kinase m2 transformation and nuclear translocation leading to suppression of aerobic glycolysis mediates Beta Elemene inhibition of breast cancer metastasis
Social Science Research Network, 2018Co-Authors: Wenxing Chen, Yanhong Pan, Wei Wang, Shuai Huang, Zhonghong Wei, Yuzhu Cao, Qi Jia, Chuan Chai, Qian Zheng, Lei ZhangAbstract:Pyruvate kinase M2 (PKM2) plays a central role in regulating aerobic glycolysis and is considered as a potential target for cancer therapy. However, its role in cancer metastasis is rarely known. Here, we found a tight relationship between PKM2 and breast cancer metastasis, which is demonstrated by the finding that Beta-Elemene (β-Elemene), an approved drug for complementary cancer therapy, exerted distinct anti-metastatic activity dependent on PKM2. The results indicated thatβ-Elemene inhibited breast cancer cell migration, invasion and angiogenesis. β-Elemene also inhibited the process of glycolysis, and decreased the utilization of glucose and the production of pyruvate and lactate through suppressing pyruvate kinase activity by modulating the transformation of dimeric and tetrameric forms of PKM2, which was reversed in part by fructose-1,6-bisphosphate (FBP) or L-cysteine. Our further analysis revealed that β-Elemene suppressed aerobic glycolysis through inhibiting the nuclear transportation of PKM2 and the expression of GLUT1, MCT1, MCT4 and LDHA by influencing the expression of importin α5. Additionally, β-Elemene remarkably inhibited the breast cancer metastases in lung and liver and selectively influenced the glycolysis of the lung and liver metastatic foci in mouse models. Taken together, tetrameric transformation and nuclear translocation of PKM2 are essential for cancer metastasis, and β-Elemene inhibits breast cancer metastasis via blocking aerobic glycolysis induced by dimeric PKM2 transformation and EGFR-importin α5 mediated PKM2 nuclear translocation, being a promising anti-metastatic agent. Funding Statement: The work was supported by National Natural Science Foundation of China (No. 81673648, 81673725, 81573859, 81603339), Natural Science Foundation of Higher School of Jiangsu Province (17KJA360003), and the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD). Declaration of Interests: The authors declare that they have no conflict of interest. Ethics Approval Statement: All animal studies were approved by the Animal Care and Use Committee of Nanjing University of Chinese Medicine. All mouse experimental procedures were performed in accordance with the Regulations for the Administration of Affairs Concerning Experimental Animals approved by the State Council of People’s Republic of China.