Overexpression of miR-215-3p sensitizes colorectal cancer to 5-fluorouracil induced apoptosis through regulating CXCR1

X.-W. Li, S.-J. Qiu, X. Zhang

Department of Clinical Laboratory, Southeast University Affiliated Zhongda Hospital, Nanjing, Jiangsu Province, China. zhangxizxi1@163.com

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• Oncology

OBJECTIVE: Chemo-resistance of colon cancer remains a major problem in therapy. The role of miR-215-3p in the chemo-sensitivity of colon cancer remains unidentified.

PATIENTS AND METHODS: Here, we constructed a 5-Fluoracil (5-Fu) resistant HCT116 cell line (HCT116/5-Fu) and miR-215-3p expression levels were measured in 56 cases of colon cancer tissues and 23 cases of normal tissues by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of miR-215-3p on colon cancer cell growth and apoptosis were investigated using cell counting kit-8 (CCK-8) and apoptosis assay, respectively. In addition, CXC-chemokine receptor type1 (CXCR1) was identified as a target of miR-215-3p by using luciferase reporter assay.

RESULTS: miR-215-3p was down-expressed in the 5-FU resistant cell compared to the parent cell. The level of miR-215-3p was correlated with the 5-Fu sensibility of colorectal cancer cell and the alteration of miR-215-3p affected the sensibility of colorectal cancer cells toward 5-Fu. Furthermore, miR-215-3p accelerated the apoptosis of colorectal cancer cell which was treated with 5-Fu. Mechanically, miR-215-3p regulated the level of endogenous CXCR1 in HCT116 cell and alternation of CXCR1 affected the 5-Fu sensibility mediated by miR-215-3p. Finally, overexpression of miR-215-3p restrained the growth of HCT116/5-Fu cells in the xenograft model.

CONCLUSIONS: MiR-215-3p improved the 5-Fu sensibility via regulating the expression of CXCR1 in the colorectal cancer cell.

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