Horm Metab Res 2015; 47(11): 861-865
DOI: 10.1055/s-0034-1398564
Endocrine Research
© Georg Thieme Verlag KG Stuttgart · New York

Glargine Promotes Human Colorectal Cancer Cell Proliferation via Upregulation of miR-95

J. Qin
1   Department of Radiation Oncology of Clinical Cancer Center, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, China
,
J.-A. Teng
2   Department of Cadre Medicine, Division of Endocrinology and Metabolism, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, China
,
Z. Zhu
3   Department of Gastrointestinal and Peripheral Vascular Surgery, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, China
,
J.-X. Chen
1   Department of Radiation Oncology of Clinical Cancer Center, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, China
,
Y.-Y. Wu
4   Department of Pharmacology, School of Pharmacy, Chengdu Medical College, Chengdu, China
› Author Affiliations
Further Information

Publication History

received 16 November 2014

accepted 18 December 2014

Publication Date:
11 February 2015 (online)

Preview

Abstract

Several studies have shown a correlation between glargine use and cancer risk. However, the role of glargine in carcinogenesis, especially in colorectal cancer (CRC), is still inconclusive. The aim of this study was to investigate the influence of glargine on proliferation of CRC cells and its possible mechanism. Effect of glargine on the cell proliferation was tested in HCT-116 and SW480 cells by MTT assay, and apoptosis was measured by flow cytometry. The expression of microRNA-95 (miR-95) and sorting nexin 1 (SNX1) protein was also determined by real-time PCR and Western blotting, respectively. The results showed that high dose glargine (from 150 to 300 nM) promoted proliferation and inhibit2ed apoptosis of CRC cells compared with untreated cells. Moreover, glargine could upregulate miR-95 and downregulate SNX1 protein expression in CRC cells. These data show that glargine may indeed trigger cellular proliferation in CRC, probably by regulating miR-95.