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Kalyan Mitra - One of the best experts on this subject based on the ideXlab platform.

  • α Solanine induces ros mediated autophagy through activation of endoplasmic reticulum stress and inhibition of akt mtor pathway
    Cell Death and Disease, 2015
    Co-Authors: Mohammad Hasanain, Arnab Bhattacharjee, Praveen Pandey, Raghib Ashraf, Neetu Singh, Sandeep K Sharma, Achchhe Lal Vishwakarma, Dipak Datta, Kalyan Mitra
    Abstract:

    α-Solanine is a glycoalkaloid found in species of the nightshade family including potato. It was primarily reported to have toxic effects in humans. However, there is a growing body of literature demonstrating in vitro and in vivo anticancer activity of α-Solanine. Most of these studies have shown activation of apoptosis as the underlying mechanism in antitumor activity of α-Solanine. In this study, we report α-Solanine as a potential inducer of autophagy, which may act synergistically or in parallel with apoptosis to exert its cytotoxic effect. Induction of autophagy was demonstrated by several assays including electron microscopy, immunoblotting of autophagy markers and immunofluorescence for LC3 (microtubule-associated protein 1 (MAP1) light chain-3) puncta. α-Solanine-induced autophagic flux was demonstrated by additionally enhanced – turnover of LC3-II and – accumulation of LC3-specific puncta after co-incubation of cells with either of the autophagolysosome inhibitors – chloroquine and – bafilomycin A1. We also demonstrated α-Solanine-induced oxidative damage in regulating autophagy where pre-incubation of cells with reactive oxygen species (ROS) scavenger resulted in suppression of CM-H2DCFDA (5 (and 6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate acetyl ester) fluorescence as well as decrease in LC3-II turnover. α-Solanine treatment caused an increase in the expression of endoplasmic reticulum (ER) stress proteins (BiP, activating transcription factor 6 (ATF6), X-box-binding protein 1, PERK, inositol-requiring transmembrane kinase/endonuclease 1, ATF4 and CCAAT-enhancer-binding protein (C/EBP)-homologous protein) suggesting activation of unfolded protein response pathway. Moreover, we found downregulation of phosphorylated Akt (Thr308 and Ser473), mammalian target of rapamycin (mTOR; Ser2448 and Ser2481) and 4E-BP1 (Thr37/46) by α-Solanine implying suppression of the Akt/mTOR pathway. Collectively, our results signify that α-Solanine induces autophagy to exert anti-proliferative activity by triggering ER stress and inhibiting Akt/mTOR signaling pathway.

  • α -Solanine induces ROS-mediated autophagy through activation of endoplasmic reticulum stress and inhibition of Akt/mTOR pathway
    Cell Death and Disease, 2015
    Co-Authors: Mohammad Hasanain, Praveen Pandey, Raghib Ashraf, Neetu Singh, Sandeep K Sharma, Achchhe Lal Vishwakarma, Dipak Datta, Kalyan Mitra, Arindam Bhattacharjee, Jayanta Sarkar
    Abstract:

    α-Solanine is a glycoalkaloid found in species of the nightshade family including potato. It was primarily reported to have toxic effects in humans. However, there is a growing body of literature demonstrating in vitro and in vivo anticancer activity of α-Solanine. Most of these studies have shown activation of apoptosis as the underlying mechanism in antitumor activity of α-Solanine. In this study, we report α-Solanine as a potential inducer of autophagy, which may act synergistically or in parallel with apoptosis to exert its cytotoxic effect. Induction of autophagy was demonstrated by several assays including electron microscopy, immunoblotting of autophagy markers and immunofluorescence for LC3 (microtubule-associated protein 1 (MAP1) light chain-3) puncta. α-Solanine-induced autophagic flux was demonstrated by additionally enhanced – turnover of LC3-II and – accumulation of LC3-specific puncta after co-incubation of cells with either of the autophagolysosome inhibitors – chloroquine and – bafilomycin A1. We also demonstrated α-Solanine-induced oxidative damage in regulating autophagy where pre-incubation of cells with reactive oxygen species (ROS) scavenger resulted in suppression of CM-H2DCFDA (5 (and 6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate acetyl ester) fluorescence as well as decrease in LC3-II turnover. α-Solanine treatment caused an increase in the expression of endoplasmic reticulum (ER) stress proteins (BiP, activating transcription factor 6 (ATF6), X-box-binding protein 1, PERK, inositol-requiring transmembrane kinase/endonuclease 1, ATF4 and CCAAT-enhancer-binding protein (C/EBP)-homologous protein) suggesting activation of unfolded protein response pathway. Moreover, we found downregulation of phosphorylated Akt (Thr308 and Ser473), mammalian target of rapamycin (mTOR; Ser2448 and Ser2481) and 4E-BP1 (Thr37/46) by α-Solanine implying suppression of the Akt/mTOR pathway. Collectively, our results signify that α-Solanine induces autophagy to exert anti-proliferative activity by triggering ER stress and inhibiting Akt/mTOR signaling pathway.

Dipak Datta - One of the best experts on this subject based on the ideXlab platform.

  • α Solanine induces ros mediated autophagy through activation of endoplasmic reticulum stress and inhibition of akt mtor pathway
    Cell Death and Disease, 2015
    Co-Authors: Mohammad Hasanain, Arnab Bhattacharjee, Praveen Pandey, Raghib Ashraf, Neetu Singh, Sandeep K Sharma, Achchhe Lal Vishwakarma, Dipak Datta, Kalyan Mitra
    Abstract:

    α-Solanine is a glycoalkaloid found in species of the nightshade family including potato. It was primarily reported to have toxic effects in humans. However, there is a growing body of literature demonstrating in vitro and in vivo anticancer activity of α-Solanine. Most of these studies have shown activation of apoptosis as the underlying mechanism in antitumor activity of α-Solanine. In this study, we report α-Solanine as a potential inducer of autophagy, which may act synergistically or in parallel with apoptosis to exert its cytotoxic effect. Induction of autophagy was demonstrated by several assays including electron microscopy, immunoblotting of autophagy markers and immunofluorescence for LC3 (microtubule-associated protein 1 (MAP1) light chain-3) puncta. α-Solanine-induced autophagic flux was demonstrated by additionally enhanced – turnover of LC3-II and – accumulation of LC3-specific puncta after co-incubation of cells with either of the autophagolysosome inhibitors – chloroquine and – bafilomycin A1. We also demonstrated α-Solanine-induced oxidative damage in regulating autophagy where pre-incubation of cells with reactive oxygen species (ROS) scavenger resulted in suppression of CM-H2DCFDA (5 (and 6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate acetyl ester) fluorescence as well as decrease in LC3-II turnover. α-Solanine treatment caused an increase in the expression of endoplasmic reticulum (ER) stress proteins (BiP, activating transcription factor 6 (ATF6), X-box-binding protein 1, PERK, inositol-requiring transmembrane kinase/endonuclease 1, ATF4 and CCAAT-enhancer-binding protein (C/EBP)-homologous protein) suggesting activation of unfolded protein response pathway. Moreover, we found downregulation of phosphorylated Akt (Thr308 and Ser473), mammalian target of rapamycin (mTOR; Ser2448 and Ser2481) and 4E-BP1 (Thr37/46) by α-Solanine implying suppression of the Akt/mTOR pathway. Collectively, our results signify that α-Solanine induces autophagy to exert anti-proliferative activity by triggering ER stress and inhibiting Akt/mTOR signaling pathway.

  • α -Solanine induces ROS-mediated autophagy through activation of endoplasmic reticulum stress and inhibition of Akt/mTOR pathway
    Cell Death and Disease, 2015
    Co-Authors: Mohammad Hasanain, Praveen Pandey, Raghib Ashraf, Neetu Singh, Sandeep K Sharma, Achchhe Lal Vishwakarma, Dipak Datta, Kalyan Mitra, Arindam Bhattacharjee, Jayanta Sarkar
    Abstract:

    α-Solanine is a glycoalkaloid found in species of the nightshade family including potato. It was primarily reported to have toxic effects in humans. However, there is a growing body of literature demonstrating in vitro and in vivo anticancer activity of α-Solanine. Most of these studies have shown activation of apoptosis as the underlying mechanism in antitumor activity of α-Solanine. In this study, we report α-Solanine as a potential inducer of autophagy, which may act synergistically or in parallel with apoptosis to exert its cytotoxic effect. Induction of autophagy was demonstrated by several assays including electron microscopy, immunoblotting of autophagy markers and immunofluorescence for LC3 (microtubule-associated protein 1 (MAP1) light chain-3) puncta. α-Solanine-induced autophagic flux was demonstrated by additionally enhanced – turnover of LC3-II and – accumulation of LC3-specific puncta after co-incubation of cells with either of the autophagolysosome inhibitors – chloroquine and – bafilomycin A1. We also demonstrated α-Solanine-induced oxidative damage in regulating autophagy where pre-incubation of cells with reactive oxygen species (ROS) scavenger resulted in suppression of CM-H2DCFDA (5 (and 6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate acetyl ester) fluorescence as well as decrease in LC3-II turnover. α-Solanine treatment caused an increase in the expression of endoplasmic reticulum (ER) stress proteins (BiP, activating transcription factor 6 (ATF6), X-box-binding protein 1, PERK, inositol-requiring transmembrane kinase/endonuclease 1, ATF4 and CCAAT-enhancer-binding protein (C/EBP)-homologous protein) suggesting activation of unfolded protein response pathway. Moreover, we found downregulation of phosphorylated Akt (Thr308 and Ser473), mammalian target of rapamycin (mTOR; Ser2448 and Ser2481) and 4E-BP1 (Thr37/46) by α-Solanine implying suppression of the Akt/mTOR pathway. Collectively, our results signify that α-Solanine induces autophagy to exert anti-proliferative activity by triggering ER stress and inhibiting Akt/mTOR signaling pathway.

Qizhao Zhou - One of the best experts on this subject based on the ideXlab platform.

  • Inhibition of prostate cancer growth by Solanine requires the suppression of cell cycle proteins and the activation of ROS/P38 signaling pathway
    Cancer Medicine, 2016
    Co-Authors: Weifeng Zhong, Zhihai Deng, Genlong Jiao, Qizhao Zhou
    Abstract:

    Solanine, a naturally steroidal glycoalkaloid in nightshade (Solanum nigrum Linn.), can inhibit proliferation and induce apoptosis of tumor cells. However, the mechanism of Solanine-suppressing prostate cancer cell growth remains to be elucidated. This study investigates the inhibition mechanism of Solanine on cancer development in vivo and in cultured human prostate cancer cell DU145 in vitro. Results show that Solanine injection significantly suppresses the tumor cell growth in xenograft athymic nude mice. Solanine regulates the protein levels of cell cycle proteins, including Cyclin D1, Cyclin E1, CDK2, CDK4, CDK6, and P21 in vivo and in vitro. Also, in cultured DU145 cell, Solanine significantly inhibits cell growth. Moreover, the administration of NAC, an active oxygen scavenger, markedly reduces Solanine-induced cell death. Blockade of P38 MAPK kinase cannot suppress reactive oxygen species (ROS), but can suppress Solanine-induced cell apoptosis. Also, inhibition of ROS by NAC inactivates P38 pathway. Taken together, the data suggest that inhibition of prostate cancer growth by Solanine may be through blocking the expression of cell cycle proteins and inducing apoptosis via ROS and activation of P38 pathway. These findings indicate an attractive therapeutic potential of Solanine for suppression of prostate cancer.

  • inhibition of prostate cancer growth by Solanine requires the suppression of cell cycle proteins and the activation of ros p38 signaling pathway
    Cancer Medicine, 2016
    Co-Authors: Weifeng Zhong, Zhihai Deng, Genlong Jiao, Qizhao Zhou
    Abstract:

    Solanine, a naturally steroidal glycoalkaloid in nightshade (Solanum nigrum Linn.), can inhibit proliferation and induce apoptosis of tumor cells. However, the mechanism of Solanine-suppressing prostate cancer cell growth remains to be elucidated. This study investigates the inhibition mechanism of Solanine on cancer development in vivo and in cultured human prostate cancer cell DU145 in vitro. Results show that Solanine injection significantly suppresses the tumor cell growth in xenograft athymic nude mice. Solanine regulates the protein levels of cell cycle proteins, including Cyclin D1, Cyclin E1, CDK2, CDK4, CDK6, and P21 in vivo and in vitro. Also, in cultured DU145 cell, Solanine significantly inhibits cell growth. Moreover, the administration of NAC, an active oxygen scavenger, markedly reduces Solanine-induced cell death. Blockade of P38 MAPK kinase cannot suppress reactive oxygen species (ROS), but can suppress Solanine-induced cell apoptosis. Also, inhibition of ROS by NAC inactivates P38 pathway. Taken together, the data suggest that inhibition of prostate cancer growth by Solanine may be through blocking the expression of cell cycle proteins and inducing apoptosis via ROS and activation of P38 pathway. These findings indicate an attractive therapeutic potential of Solanine for suppression of prostate cancer.

Mohammad Hasanain - One of the best experts on this subject based on the ideXlab platform.

  • α Solanine induces ros mediated autophagy through activation of endoplasmic reticulum stress and inhibition of akt mtor pathway
    Cell Death and Disease, 2015
    Co-Authors: Mohammad Hasanain, Arnab Bhattacharjee, Praveen Pandey, Raghib Ashraf, Neetu Singh, Sandeep K Sharma, Achchhe Lal Vishwakarma, Dipak Datta, Kalyan Mitra
    Abstract:

    α-Solanine is a glycoalkaloid found in species of the nightshade family including potato. It was primarily reported to have toxic effects in humans. However, there is a growing body of literature demonstrating in vitro and in vivo anticancer activity of α-Solanine. Most of these studies have shown activation of apoptosis as the underlying mechanism in antitumor activity of α-Solanine. In this study, we report α-Solanine as a potential inducer of autophagy, which may act synergistically or in parallel with apoptosis to exert its cytotoxic effect. Induction of autophagy was demonstrated by several assays including electron microscopy, immunoblotting of autophagy markers and immunofluorescence for LC3 (microtubule-associated protein 1 (MAP1) light chain-3) puncta. α-Solanine-induced autophagic flux was demonstrated by additionally enhanced – turnover of LC3-II and – accumulation of LC3-specific puncta after co-incubation of cells with either of the autophagolysosome inhibitors – chloroquine and – bafilomycin A1. We also demonstrated α-Solanine-induced oxidative damage in regulating autophagy where pre-incubation of cells with reactive oxygen species (ROS) scavenger resulted in suppression of CM-H2DCFDA (5 (and 6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate acetyl ester) fluorescence as well as decrease in LC3-II turnover. α-Solanine treatment caused an increase in the expression of endoplasmic reticulum (ER) stress proteins (BiP, activating transcription factor 6 (ATF6), X-box-binding protein 1, PERK, inositol-requiring transmembrane kinase/endonuclease 1, ATF4 and CCAAT-enhancer-binding protein (C/EBP)-homologous protein) suggesting activation of unfolded protein response pathway. Moreover, we found downregulation of phosphorylated Akt (Thr308 and Ser473), mammalian target of rapamycin (mTOR; Ser2448 and Ser2481) and 4E-BP1 (Thr37/46) by α-Solanine implying suppression of the Akt/mTOR pathway. Collectively, our results signify that α-Solanine induces autophagy to exert anti-proliferative activity by triggering ER stress and inhibiting Akt/mTOR signaling pathway.

  • α -Solanine induces ROS-mediated autophagy through activation of endoplasmic reticulum stress and inhibition of Akt/mTOR pathway
    Cell Death and Disease, 2015
    Co-Authors: Mohammad Hasanain, Praveen Pandey, Raghib Ashraf, Neetu Singh, Sandeep K Sharma, Achchhe Lal Vishwakarma, Dipak Datta, Kalyan Mitra, Arindam Bhattacharjee, Jayanta Sarkar
    Abstract:

    α-Solanine is a glycoalkaloid found in species of the nightshade family including potato. It was primarily reported to have toxic effects in humans. However, there is a growing body of literature demonstrating in vitro and in vivo anticancer activity of α-Solanine. Most of these studies have shown activation of apoptosis as the underlying mechanism in antitumor activity of α-Solanine. In this study, we report α-Solanine as a potential inducer of autophagy, which may act synergistically or in parallel with apoptosis to exert its cytotoxic effect. Induction of autophagy was demonstrated by several assays including electron microscopy, immunoblotting of autophagy markers and immunofluorescence for LC3 (microtubule-associated protein 1 (MAP1) light chain-3) puncta. α-Solanine-induced autophagic flux was demonstrated by additionally enhanced – turnover of LC3-II and – accumulation of LC3-specific puncta after co-incubation of cells with either of the autophagolysosome inhibitors – chloroquine and – bafilomycin A1. We also demonstrated α-Solanine-induced oxidative damage in regulating autophagy where pre-incubation of cells with reactive oxygen species (ROS) scavenger resulted in suppression of CM-H2DCFDA (5 (and 6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate acetyl ester) fluorescence as well as decrease in LC3-II turnover. α-Solanine treatment caused an increase in the expression of endoplasmic reticulum (ER) stress proteins (BiP, activating transcription factor 6 (ATF6), X-box-binding protein 1, PERK, inositol-requiring transmembrane kinase/endonuclease 1, ATF4 and CCAAT-enhancer-binding protein (C/EBP)-homologous protein) suggesting activation of unfolded protein response pathway. Moreover, we found downregulation of phosphorylated Akt (Thr308 and Ser473), mammalian target of rapamycin (mTOR; Ser2448 and Ser2481) and 4E-BP1 (Thr37/46) by α-Solanine implying suppression of the Akt/mTOR pathway. Collectively, our results signify that α-Solanine induces autophagy to exert anti-proliferative activity by triggering ER stress and inhibiting Akt/mTOR signaling pathway.

Maryam Mohsenikia - One of the best experts on this subject based on the ideXlab platform.

  • therapeutic effects of dendrosomal Solanine on a metastatic breast tumor
    Life Sciences, 2016
    Co-Authors: Maryam Mohsenikia, Ali Mohammad Alizadeh, Saeed Khodayari, Hamid Khodayari, Baharak Farhangi, Vahid Khori, Yasaman Arjmand Abbassi, Milica Vesovic, Ali Soleymani, Farhood Najafi
    Abstract:

    Abstract Aims Our previous studies showed that alpha-Solanine can inhibit tumor growth in cell culture and animal models of breast cancer. However, Solanine is insoluble in common solvents; therefore, we developed a special nanoparticle with high-capacity solubility. The present study is aimed to deliberate the therapeutic effects of dendrosomal Solanine (DNS) on a metastatic breast tumor in vitro and in vivo . Main methods After DNS preparation and dosing procedures, forty-five mice were equally divided into five groups to investigate the anti-metastatic effects of DNS on mammary tumor-bearing mice. Key findings Compared to Solanine, DNS significantly suppressed the proliferation of 4 T1 cells in a dose- and time-dependent manner. DNS showed a remarkable safety rate of up to 10 mg/kg. A significant decrease in white blood-cell count was seen at 20 mg/kg DNS in comparison with control animals. Mice treated with DNS had smaller tumor volume (mm 3 ) in comparison with control and Solanine groups. Moreover, the incidence of the breast tumor metastases was about 67% in the control animals, where as Solanine and DNS 1 mg/kg were about 22% and 0%, respectively. Furthermore, the number of metastases per mouse varied from one to three. The tissues of tumor, brain, liver, spleen, and lung showed higher expression levels of Bcl-2 but lower expression levels of Bax, MMP-2, MMP-9, mTOR, and Akt in DNS-treated mice than control and Solanine groups. Significance The findings suggest that DNS has a more impactful therapeutic effect than Solanine on 4 T1-induced breast tumorigenesis via influencing the tissue microenvironment.

  • the protective and therapeutic effects of alpha Solanine on mice breast cancer
    European Journal of Pharmacology, 2013
    Co-Authors: Maryam Mohsenikia, Ali Mohammad Alizadeh, Saeed Khodayari, Hamid Khodayari, Seyed Amin Kouhpayeh, Aliasghar Karimi, Mina Zamani, Saleh Azizian, Mohammad Ali Mohagheghi
    Abstract:

    Abstract Alpha-Solanine, a naturally steroidal glycoalkaloid, is found in leaves and fruits of plants as a defensive agent against fungi, bacteria and insects. Herein, we investigated Solanine toxicity in vitro and in vivo , and assessed its protective and the therapeutic effects on a typical animal model of breast cancer. The study conducted in three series of experiments to obtain (i) Solanine effects on cell viability of mammary carcinoma cells, (ii) in vivo toxicity of Solanine, and (iv) the protective and therapeutic effects of Solanine on animal model of breast cancer. Alpha-Solanine significantly suppressed proliferation of mouse mammary carcinoma cells both in vitro and in vivo ( P P P P P P