Literature DB >> 29397517

Do MCF7 cells cope with metformin treatment under energetic stress in low glucose conditions?

Irem Dogan Turacli1, Haldun Umudum2, Arzu Pampal3, Tuba Candar4, Lara Kavasoglu5, Yaren Sari5.   

Abstract

There is a growing body of evidence about metformin being effective in cancer therapy. Despite controversies about the ways of its effectiveness, several ongoing clinical trials are evaluating the drug when used as an adjuvant or a neo-adjuvant agent. We aimed to investigate metformin's effects on proliferation, metastasis, and hormone receptor expressions in breast cancer cell line MCF-7 incubated in two different glucose conditions. MCF-7 cells were incubated in high or low glucose media and treated with various doses of metformin. The cell viability was studied using MTT test. The Ki-67, estrogen and progesterone receptor expression were evaluated by ICC and galectin-3 expression was evaluated by ELISA or spectrophotometrically. The cell viability following consecutive metformin doses in either glucose condition for 24 and 48 h represented a significant decrease when compared to control. The proliferation detected in low glucose medium following metformin at doses < 20 mM was found significantly decreased when compared to high glucose medium at 48 h. In terms of galectin-3 levels, the increase in high glucose medium treated with metformin and the decrease in low glucose medium were found statistically significant when compared to control. Progesterone receptor staining demonstrated a significant increase in low glucose medium. Our findings represent better outcomes for cancer lines incubated in low glucose medium treated with metformin in terms of viability, receptor expression and metastatic activity, and highlight the potential benefit of metformin especially in restraining the cancer cell's ability to cope energetic stress in low glucose conditions.

Entities:  

Keywords:  Breast cancer; Estrogen receptor; Galectin-3; Low glucose; Metformin; Progesterone receptor

Mesh:

Substances:

Year:  2018        PMID: 29397517     DOI: 10.1007/s11033-018-4152-5

Source DB:  PubMed          Journal:  Mol Biol Rep        ISSN: 0301-4851            Impact factor:   2.316


  36 in total

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Review 3.  Targeting mitochondria metabolism for cancer therapy.

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Journal:  Biochem Biophys Res Commun       Date:  2012-11-15       Impact factor: 3.575

Review 5.  The Warburg Effect: How Does it Benefit Cancer Cells?

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7.  High glucose promotes pancreatic cancer cell proliferation via the induction of EGF expression and transactivation of EGFR.

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8.  Insulin-like growth factor (IGF) signaling in tumorigenesis and the development of cancer drug resistance.

Authors:  Sahitya K Denduluri; Olumuyiwa Idowu; Zhongliang Wang; Zhan Liao; Zhengjian Yan; Maryam K Mohammed; Jixing Ye; Qiang Wei; Jing Wang; Lianggong Zhao; Hue H Luu
Journal:  Genes Dis       Date:  2015-03-01

9.  Histological evaluation of AMPK signalling in primary breast cancer.

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10.  A combinatorial extracellular matrix platform identifies cell-extracellular matrix interactions that correlate with metastasis.

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Journal:  Nat Commun       Date:  2012       Impact factor: 14.919

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  2 in total

1.  Potential intrinsic subtype dependence on the association between metformin use and survival in surgically resected breast cancer: a Korean national population-based study.

Authors:  Byoung Hyuck Kim; Moon-June Cho; Jeanny Kwon
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2.  The Effect of Metformin on the Clinicopathological Features of Breast Cancer With Type 2 Diabetes.

Authors:  Weili Min; Baofeng Wang; Aining Guo; Guochao Mao; Yang Zhao; Shuqun Zhang; Rui He; Yihe Min; Yi Huang
Journal:  World J Oncol       Date:  2020-02-02
  2 in total

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