Literature DB >> 22540333

Metformin sensitizes endometrial cancer cells to chemotherapy by repressing glyoxalase I expression.

Lingling Dong1, Qian Zhou, Zhenbo Zhang, Yaping Zhu, Tao Duan, Youji Feng.   

Abstract

AIM: Metformin plays an important role in the inhibition of cancer cell growth and prolongs remission durations. It reverses progestin-resistance in endometrial cancer cells by downregulating glyoxalase I (GloI) expression. This study aimed to investigate the effect of metformin on endometrial cancer cell chemotherapeutic sensitivity and explore the underlying molecular mechanisms.
MATERIAL AND METHODS: MTT assay was performed to determine the rate of cell death after cisplatin and paclitaxel with or without metformin. Western blot was carried out to analyze GloI expression. SiRNA-targeting of GloI was used to knockdown GloI expression before further treatment with chemotherapeutic agents to examine the effect of GloI downregulation on chemotherapy-induced cell killing. In addition, plasmid transfection was used to overexpress GloI and determine whether high GloI levels blocked metformin-enhanced cell sensitivity to chemotherapy. PCR was used to analyze the efficiency of RNA interference and plasmid transfection.
RESULTS: The addition of metformin enhanced the sensitivity of endometrial cells to cisplatin and paclitaxel, which was associated with reduced levels of GloI expression. Moreover, low-dose chemotherapeutic drugs alone could not significantly reduce GloI expression, whereas the addition of metformin potently downregulated GloI protein levels. Cisplatin and paclitaxel markedly inhibited the proliferative ability of GloI-depleted endometrial cancer cells. However, the overexpression of GloI abolished the effect of metformin-enhanced cell sensitivity to chemotherapeutic drugs.
CONCLUSION: Metformin enhances the rate of cell-killing induced by chemotherapeutic agents by repressing GloI expression.
© 2012 The Authors. Journal of Obstetrics and Gynaecology Research © 2012 Japan Society of Obstetrics and Gynecology.

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Year:  2012        PMID: 22540333     DOI: 10.1111/j.1447-0756.2011.01839.x

Source DB:  PubMed          Journal:  J Obstet Gynaecol Res        ISSN: 1341-8076            Impact factor:   1.730


  25 in total

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