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Drug: Metformin

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Total 134 results found since Jan 2013.

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

Involvement of the AMPK-PTEN pathway in insulin resistance induced by high glucose in cultured rat podocytes.
Abstract As part of the filtration barrier, podocytes play an important role in the development of diabetic nephropathy. Disturbances in insulin signaling accompanied by insulin resistance can lead to various intracellular events. We hypothesized that high glucose concentrations would lead to disturbances in interactions between AMPK and PTEN proteins in podocytes. Experiments were performed in primary rat podocytes cultured with normal (5.6mM) or high (30mM) glucose concentrations for 5 d. Immunodetection methods were used to detect AMPK, PTEN, insulin receptor, and Akt proteins, and their phosphorylated forms. I...
Source: The International Journal of Biochemistry and Cell Biology - April 15, 2014 Category: Biochemistry Authors: Rogacka D, Piwkowska A, Audzeyenka I, Angielski S, Jankowski M Tags: Int J Biochem Cell Biol 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

Metformin induces PGC‐1α expression and selectively affects hepatic PGC‐1α functions
Conclusions and ImplicationsDownregulation of PGC‐1α is not necessary for suppression of gluconeogenic genes by metformin. Importantly, metformin selectively regulates hepatic PGC‐1α‐mediated gene regulation and prevents activation of gluconeogenesis, but leaves regulation of mitochondrial genes intact. Our results thus identify selective modulation of hepatic PGC‐1α functions as a novel mechanism involved in the therapeutic action of metformin.
Source: British Journal of Pharmacology - January 16, 2014 Category: Drugs & Pharmacology Authors: Sanna‐Mari Aatsinki, Marcin Buler, Henriikka Salomäki, Markku Koulu, Petr Pavek, Jukka Hakkola Tags: Research Paper 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

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

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

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

AMP-activated protein kinase inhibits TGF-β-, angiotensin II-, aldosterone-, high glucose- and albumin-induced epithelial-mesenchymal transition.
In conclusion, AMPK activation might be beneficial in attenuating the tubulointerstitial fibrosis induced by TGF-β, angiotensin II, aldosterone, high glucose and urinary albumin. PMID: 23324179 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Renal Physiology - January 16, 2013 Category: Physiology Authors: Lee JH, Kim JH, Kim JS, Chang JW, Kim SB, Park JS, Lee SK Tags: Am J Physiol Renal Physiol Source Type: research

Metformin-mediated downregulation of p38 mitogen-activated protein kinase-dependent excision repair cross-complementing 1 decreases DNA repair capacity and sensitizes human lung cancer cells to paclitaxel.
Abstract Metformin, an extensively used and well-tolerated drug for treating individuals with type 2 diabetes, has recently gained significant attention as an anticancer drug. On the other hand, paclitaxel (Taxol) is a new antineoplastic drug that has shown promise in the treatment of non-small cell lung cancer (NSCLC). High expression levels of excision repair cross-complementary 1 (ERCC1) in cancers have been positively associated with the DNA repair capacity and a poor prognosis in NSCLC patients treated with platinum-containing chemotherapy. In this current study, paclitaxel was found to increase phosphorylati...
Source: Biochemical Pharmacology - December 7, 2012 Category: Drugs & Pharmacology Authors: Tseng SC, Huang YC, Chen HJ, Chiu HC, Huang YJ, Wo TY, Weng SH, Lin YW Tags: Biochem Pharmacol Source Type: research