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Total 133 results found since Jan 2013.

Abstract 4969: Metformin causes AR degradation via Skp2-mediated ubiquitination
This study supports that use of metformin in combination with Enza or other ARSI drugs may not only block autophagy survival but also cause AR degradation that leads to PC cell death.Citation Format: Joy C. Yang, Allen C. Gao, Christopher P. Evans. Metformin causes AR degradation via Skp2-mediated ubiquitination. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4969. doi:10.1158/1538-7445.AM2015-4969
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Yang, J. C., Gao, A. C., Evans, C. P. Tags: Molecular and Cellular Biology Source Type: research

Abstract 3814: Metformin induces ER stress-dependent apoptosis through miR-708-5p/NNAT pathway in prostate cancer
In this study, we identified miR-708-5p as a novel downstream effector of metformin in prostate cancer. By increasing the expression of miR-708-5p, metformin suppresses the expression of endoplasmic reticulum (ER) membrane protein neuronatin (NNAT) and subsequently induces apoptosis of prostate cancer cells through ER stress pathway. Notably, down-regulated NNAT is associated with down-regulated intracellular calcium level and induces malformation of endoplasmic reticulum-ribosome structure which is revealed by electronic microscopy. Furthermore, western blot shows that the unfolded-protein response (UPR) proteins includin...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Yang, J., Wei, J., Wu, Y., Wang, Z., Guo, Y., Li, X. Tags: Molecular and Cellular Biology Source Type: research

Impact of AMPK on Glucosylceramide Metabolism Glycobiology and Extracellular Matrices
The membrane glycolipid glucosylceramide (GlcCer) plays a critical role in cellular homeostasis. Its intracellular levels are thought to be tightly regulated. How cells regulate GlcCer levels remains to be clarified. AMP-activated protein kinase (AMPK), which is a crucial cellular energy sensor, regulates glucose and lipid metabolism to maintain energy homeostasis. Here, we investigated whether AMPK affects GlcCer metabolism. AMPK activators (5-aminoimidazole-4-carboxamide 1-β-d-ribofuranoside and metformin) decreased intracellular GlcCer levels and synthase activity in mouse fibroblasts. AMPK inhibitors or AMPK siRNA rev...
Source: Journal of Biological Chemistry - July 16, 2015 Category: Chemistry Authors: Ishibashi, Y., Hirabayashi, Y. Tags: Lipids Source Type: research

Activation of AMP-Activated Protein Kinase Prevents TGF-β1-Induced Epithelial-Mesenchymal Transition and Myofibroblast Activation.
Abstract Transforming growth factor (TGF)-β contributes to tubulointerstitial fibrosis. We investigated the mechanism by which TGF-β exerts its profibrotic effects and specifically the role of AMP-activated protein kinase (AMPK) in kidney tubular epithelial cells and interstitial fibroblasts. In proximal tubular epithelial cells, TGF-β1 treatment causes a decrease in AMPK phosphorylation and activation together with increased fibronectin and α-smooth muscle actin expression and decreased in E-cadherin. TGF-β1 causes similar changes in interstitial fibroblasts. Activation of AMPK with5-aminoimidazole-4-carboxa...
Source: The American Journal of Pathology - June 9, 2015 Category: Pathology Authors: Thakur S, Viswanadhapalli S, Kopp JB, Shi Q, Block K, Gorin Y, Abboud HE Tags: Am J Pathol Source Type: research

Metformin exerts anticancer effects through the inhibition of the Sonic hedgehog signaling pathway in breast cancer.
Abstract Metformin, a widely prescribed antidiabetic drug, has previously been shown to lower the risk of certain types of cancer, including that of breast cancer, and to improve prognosis. Its anticancer effects, which are mediated by the activation of AMP-activated protein kinase (AMPK), have become notable. The Sonic hedgehog (Shh) signaling pathway is involved in changes in mammary ducts and malignant transformation. The aim of the present study was to elucidate the role of the Shh pathway in mediating the anticancer effects of metformin and the correlation between AMPK and the Shh pathway. We investigated t...
Source: International Journal of Molecular Medicine - May 21, 2015 Category: Molecular Biology Authors: Fan C, Wang Y, Liu Z, Sun Y, Wang X, Wei G, Wei J Tags: Int J Mol Med 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

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

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

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

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

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. PMID: 25428127 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Renal Physiology - November 26, 2014 Category: Physiology Authors: Kim H, Moon SY, Kim JS, Baek CH, Kim M, Min JY, Lee SK Tags: Am J Physiol Renal Physiol 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

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

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

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