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Drug: Metformin

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Total 134 results found since Jan 2013.

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

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

Polycystin-1 but not polycystin-2 deficiency causes upregulation of the mTOR pathway and can be synergistically targeted with rapamycin and metformin.
Abstract Autosomal dominant polycystic kidney disease (ADPKD) is caused by loss-of-function mutations in either PKD1 or PKD2 genes, which encode polycystin-1 (TRPP1) and polycystin-2 (TRPP2), respectively. Increased activity of the mammalian target of rapamycin (mTOR) pathway has been shown in PKD1 mutants but is less documented for PKD2 mutants. Clinical trials using mTOR inhibitors were disappointing, while the AMP-activated kinase (AMPK) activator, metformin is not yet tested in patients. Here, we studied the mTOR activity and its upstream pathways in several human and mouse renal cell models with either siRNA ...
Source: Pflugers Archiv : European Journal of Physiology - November 6, 2013 Category: Physiology Authors: Mekahli D, Decuypere JP, Sammels E, Welkenhuyzen K, Schoeber J, Audrezet MP, Corvelyn A, Dechênes G, Ong AC, Wilmer MJ, van den Heuvel L, Bultynck G, Parys JB, Missiaen L, Levtchenko E, De Smedt H Tags: Pflugers Arch Source Type: research

Ferritin heavy chain as main mediator of preventive effect of metformin on mitochondrial damage induced by doxorubicin in cardiomyocyte.
In conclusion, these results deepen our knowledge of the protective action of MET against DOX-induced cardiotoxicity and suggest that therapeutic strategies based on FHC modulation could protect cardiomyocytes from the mitochondrial damage induced by DOX by restoring iron homeostasis. PMID: 24231192 [PubMed - as supplied by publisher]
Source: Free Radical Biology and Medicine - November 11, 2013 Category: Biology Authors: Asensio-Lopez MC, Sanchez-Mas J, Pascual-Figal DA, de Torre C, Valdes M, Lax A Tags: Free Radic Biol Med 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

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

Small Heterodimer Partner Blocks Cardiac Hypertrophy by Interfering with GATA6 Signaling.
Conclusions: These results establish SHP as a novel anti-hypertrophic regulator that acts by interfering with GATA6 signaling. SHP may participate in the metformin-induced anti-hypertrophic response. PMID: 25015078 [PubMed - as supplied by publisher]
Source: Circulation Research - July 11, 2014 Category: Cardiology Authors: Nam YS, Kim Y, Joung H, Kwon DH, Choe N, Min HK, Kim Y, Kim HS, Kim DK, Cho YK, Kim YH, Nam KI, Choi HC, Park DH, Suk K, Lee IK, Ahn Y, Lee CH, Choi HS, Eom GH, Kook H Tags: Circ Res 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

Metformin promotes irisin release from murine skeletal muscle independently of AMPK activation
ConclusionMetformin promotes irisin release from murine skeletal muscle into blood, independently of AMPK pathway activation. Our results suggest that stimulation of irisin may be a novel molecular mechanism of metformin which is widely used for treatment of metabolic disorders.This article is protected by copyright. All rights reserved.
Source: Acta Physiologica - November 11, 2014 Category: Physiology Authors: Dong‐Jie Li, Fang Huang, Wen‐Jie Lu, Guo‐Jun Jiang, Ya‐ping Deng, Fu‐Ming Shen Tags: Regular Paper Source Type: research

Metformin promotes irisin release from murine skeletal muscle independently of AMP‐activated protein kinase activation
ConclusionMetformin promotes irisin release from murine skeletal muscle into blood, independently of AMPK pathway activation. Our results suggest that stimulation of irisin may be a novel molecular mechanism of metformin which is widely used for treatment of metabolic disorders.
Source: Acta Physiologica - November 24, 2014 Category: Physiology Authors: D.‐J. Li, F. Huang, W.‐J. Lu, G.‐J. Jiang, Y.‐P. Deng, F.‐M. Shen Tags: Original Article Source Type: research

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

Metformin inhibits TGF-b-induced myofibroblast differentiation through AMPK activation
Conclusion:Metformin suppresses NOX4 expression and ROS production via AMPK activation, resulting in inhibition of TGF-b-induced myofibroblast differentiation. Therefore, metformin may also be used for the treatment of IPF.
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Takasaka, N., Araya, J., Kurita, Y., Kobayashi, K., Ito, S., Wakui, H., Yoshii, Y., Minagawa, S., Kojima, J., Hara, H., Numata, T., Shimizu, K., Kawaishi, M., Kaneko, Y., Nakayama, K., Kuwano, K. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research

Activation of AMP-activated protein kinase inhibits ER stress and renal fibrosis
In conclusion, AMPK may serve as a promising therapeutic target through reducing ER stress and renal fibrosis.
Source: AJP: Renal Physiology - February 1, 2015 Category: Urology & Nephrology Authors: Kim, H., Moon, S. Y., Kim, J.-S., Baek, C. H., Kim, M., Min, J. Y., Lee, S. K. Tags: ARTICLES Source Type: research

Activation of AMPK by metformin inhibits TGF-β-induced collagen production in mouse renal fibroblasts
This study suggests that activation of AMPK might be a novel strategy for the treatment of chronic kidney disease (CKD) partially by inhibition of renal interstitial fibrosis (RIF).
Source: Life Sciences - March 4, 2015 Category: Biology Source Type: research

Metformin inhibits the proliferation of human prostate cancer PC-3 cells via the downregulation of insulin-like growth factor 1 receptor.
Abstract Metformin is a biguanide drug that is widely used for the treatment of type 2 diabetes. Recent studies have shown that metformin inhibits cancer cell proliferation and tumor growth both in vitro and in vivo. The anti-tumor mechanisms of metformin include activation of the AMP-activated protein kinase/mTOR pathway and direct inhibition of insulin/insulin-like growth factor (IGF)-mediated cellular proliferation. However, the anti-tumor mechanism in prostate cancer remains unclear. Because activation of the IGF-1 receptor (IGF-1R) is required for prostate cell proliferation, IGF-1R inhibitors may be of the...
Source: Biochemical and Biophysical Research communications - April 7, 2015 Category: Biochemistry Authors: Kato H, Sekine Y, Furuya Y, Miyazawa Y, Koike H, Suzuki K Tags: Biochem Biophys Res Commun Source Type: research