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AMPK/mTOR-Mediated Inhibition of Survivin Partly Contributes to Metformin-Induced Apoptosis in Human Gastric Cancer Cell.
Abstract Abstract Recent studies demonstrated that metformin exerts anti-neoplastic effect in a spectrum of malignancies. However, the mechanism whereby metformin affects various cancers, including gastric cancer, is poorly elucidated. Considering apoptosis plays critical role in tumorigenesis, we, in the present study, investigated the in vitro apoptotic effect of metformin on human gastric cancer cell and the underlying mechanism. Three differently-differentiated gastric cancer cell lines, MKN-28, SGC-7901 and BGC-823, along with one noncancerous gastric cell line GES-1 were used. We found that metformin treatme...
Source: Cancer Biology and Therapy - December 2, 2014 Category: Cancer & Oncology Authors: Han G, Gong H, Wang Y, Guo S, Liu K Tags: Cancer Biol Ther Source Type: research

Role of AMPK in Regulating EMT
In cancer cells, the epithelial–mesenchymal transition (EMT) confers the ability to invade basement membranes and metastasize to distant sites, establishing it as an appealing target for therapeutic intervention. Here, we report a novel function of the master metabolic kinase AMPK in suppressing EMT by modulating the Akt–MDM2–Foxo3 signaling axis. This mechanistic link was supported by the effects of siRNA-mediated knockdown and pharmacologic activation of AMPK on epithelial and mesenchymal markers in established breast and prostate cancer cells. Exposure of cells to OSU-53, a novel allosteric AMPK activator, as well...
Source: Cancer Research - September 1, 2014 Category: Cancer & Oncology Authors: Chou, C.-C., Lee, K.-H., Lai, I.-L., Wang, D., Mo, X., Kulp, S. K., Shapiro, C. L., Chen, C.-S. Tags: Therapeutics, Targets, and Chemical Biology Source Type: research

Repression of phosphoinositide-dependent protein kinase 1 expression by ciglitazone via Egr-1 represents a new approach for inhibition of lung cancer cell growth
Conclusion: Collectively, our results demonstrate that ciglitazone inhibits PDK1 expression through AMPKalpha-mediated induction of Egr-1 and Egr-1 binding to the specific DNA site in the PDK1 gene promoter, which is independent of PPARgamma. Activation of AMPKalpha by metformin enhances the effect of ciglitazone. In turn, this leads to inhibition of NSCLC cell proliferation.
Source: Epidemiologic Perspectives and Innovations - June 13, 2014 Category: Epidemiology Authors: SWei Sunny HannQing TangFang ZhengShunyu ZhaoJianping ChenZhiYu Wang Source Type: research

Metformin anti-tumor effect via disruption of the MID1 translational regulator complex and AR downregulation in prostate cancer cells
Conclusions: Findings reported herein uncover a mechanism for the anti-tumor activity of metformin in prostate cancer, which is independent of its anti-diabetic effects. These data provide a rationale for the use of metformin in the treatment of hormone naive and castration-resistant prostate cancer and suggest AR is an important indirect target of metformin.
Source: BMC Cancer - January 31, 2014 Category: Cancer & Oncology Authors: Ummuhan DemirAndrea KoehlerRainer SchneiderSusann SchweigerHelmut Klocker Source Type: research

Regulation of metformin response by breast cancer associated gene 2.
Abstract Adenosine monophosphate-activated protein kinase (AMPK), a master regulator of cellular energy homeostasis, has emerged as a promising molecular target in the prevention of breast cancer. Clinical trials using the United States Food and Drug Administration (FDA)-approved, AMPK-activating, antidiabetic drug metformin are promising in this regard, but the question of why metformin is protective for some women but not others still remains. Breast cancer associated gene 2 (BCA2/Rabring7/RNF115), a novel Really Interesting New Gene (RING) finger ubiquitin E3 ligase, is overexpressed in >50% of breast tumors...
Source: Neoplasia - December 1, 2013 Category: Cancer & Oncology Authors: Buac D, Kona FR, Seth AK, Dou QP Tags: Neoplasia Source Type: research

Inhibition of p38 MAPK-dependent MutS homologue-2 (MSH2) expression by metformin enhances gefitinib-induced cytotoxicity in human squamous lung cancer cells
Conclusion: Together, down-regulation of MSH2 expression can be a possible strategy to enhance the sensitivity of gefitinib to human lung squamous cancer cells.
Source: Lung Cancer - October 17, 2013 Category: Cancer & Oncology Authors: Jen-Chung Ko, Hsien-Chun Chiu, Ting-Yu Wo, Yi-Jhen Huang, Sheng-Chieh Tseng, Yu-Ching Huang, Huang-Jen Chen, Jhan-Jhang Syu, Chien-Yu Chen, Yun-Ting Jian, Yi-Jun Jian, Yun-Wei Lin Tags: Carcinogenesis and molecular biology Source Type: research

The interplay of AMP‐activated protein kinase and androgen receptor in prostate cancer cells
Abstract AMP‐activated protein kinase (AMPK) has recently emerged as a potential target for cancer therapy due to the observation that activation of AMPK inhibits tumor cell growth. It is well‐known that androgen receptor (AR) signaling is a major driver for the development and progression of prostate cancer and that downregulation of AR is a critical step in the induction of apoptosis in prostate cancer cells. However, little is known about the potential interaction between AMPK and AR signaling pathways. In the current study, we showed that activation of AMPK by metformin caused decrease of AR protein level through s...
Source: Journal of Cellular Physiology - October 17, 2013 Category: Cytology Authors: Min Shen, Zhen Zhang, Manohar Ratnam, Q. Ping Dou Tags: Rapid Communication Source Type: research

Metformin Enhances Cisplatin Cytotoxicity by Suppressing Stat3 Activity Independently of the LKB1-AMPK Pathway.
This study demonstrated a correlation between Stat3 phosphorylation and cisplatin cytotoxicity using AS2 (PC14PE6/AS2)-derived cell lines (AS2/S3C) that contained constitutively active Stat3 plasmids as a model. A Stat3 inhibitor (JSI-124) enhanced the cisplatin sensitivity in AS2 cells, whereas metformin inhibited Stat3 phosphorylation and enhanced cisplatin cytotoxicity. By contrast, another AMPK activator (AICAR) failed to produce these effects. LKB1-AMPK silencing by siRNA or mTOR inhibition by rapamycin or pp242 did not alter the effect of metformin on Stat3 activity suppression, suggesting that metformin can modulate...
Source: American Journal of Respiratory Cell and Molecular Biology - March 22, 2013 Category: Molecular Biology Authors: Lin CC, Yeh HH, Huang WL, Yan JJ, Lai WW, Su WP, Chen HH, Su WC Tags: Am J Respir Cell Mol Biol Source Type: research

Metformin Induces Cytotoxicity by Down‐Regulating Thymidine Phosphorylase and Excision Repair Cross‐Complementation 1 Expression in Non‐Small Cell Lung Cancer Cells
In conclusion, metformin induces cytotoxicity by down‐regulating TP and ERCC1 expression in NSCLC cells.
Source: Basic and Clinical Pharmacology and Toxicology - March 21, 2013 Category: Drugs & Pharmacology Authors: Jen‐Chung Ko, Yu‐Ching Huang, Huang‐Jen Chen, Sheng‐Chieh Tseng, Hsien‐Chun Chiu, Ting‐Yu Wo, Yi‐Jhen Huang, Shao‐Hsing Weng, Robin Y. Y. Chiou, Yun‐Wei Lin Tags: Original Article Source Type: research

Metformin Induces Cytotoxicity by Down‐Regulating Thymidine Phosphorylase and ERCC1 Expression in Non‐Small Cell Lung Cancer Cells
In conclusion, metformin induces cytotoxicity by down‐regulating TP and ERCC1 expression in NSCLC cells.
Source: Basic and Clinical Pharmacology and Toxicology - January 31, 2013 Category: Drugs & Pharmacology Authors: Jen‐Chung Ko, Yu‐Ching Huang, Huang‐Jen Chen, Sheng‐Chieh Tseng, Hsien‐Chun Chiu, Ting‐Yu Wo, Yi‐Jhen Huang, Shao‐Hsing Weng, Robin Y.Y. Chiou, Yun‐Wei Lin Tags: Original Article Source Type: research

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