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MiR‐216a‐3p inhibits colorectal cancer cell proliferation through direct targeting COX‐2 and ALOX5
Author(s) -
Wang Dongxia,
Li Yuechun,
Zhang Chun,
Li Xianming,
Yu Jinming
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26336
Subject(s) - microrna , colorectal cancer , cancer research , cell growth , ectopic expression , cancer , biology , medicine , cell culture , gene , genetics
Colorectal Cancer (CRC) is a most common digestive system malignant tumor. Despite recent advance in CRC treatment, searching for efficient biomarker and individual treatment therapy remains an urgent need. Cyclooxygenase‐2 (COX‐2) plays a critical role in the development and progression of CRC. In addition, shunting of arachidonic acid metabolism to the 5‐lipoxygenase (ALOX5, 5‐LO) pathway has also been reported to be implicated in the CRC pathogenesis. Cancer cell viability is promoted by ALOX5 through several mechanisms that are similar to those of COX‐2. In recent years, it has been widely recognized that through inhibition of target genes, miRNAs can exert both oncogenic and tumor suppressive functions, depending on circumstances. In the present study, we screened for candidate microRNAs (miRNAs) which were predicted to regulate COX‐2 and ALOX5 by online tools. Among the candidate miRNAs, miR‐216a‐3p expression was down‐regulated in CRC tissues and cell lines; a higher miR‐216a‐3p expression was correlated with longer overall survival in patients with CRC. Moreover, ectopic miR‐216a‐3p expression significantly suppressed CRC cell proliferation. Using luciferase reporter gene, real‐time PCR, and western blot assays, we confirmed the miR‐216a‐3p regulation of COX‐2 and ALOX5 through direct targeting; further verified that miR‐216a‐3p could inhibit COX‐2 and ALOX5 expression in CRC cells, thus to affect CRC cell proliferation. Taken together, miR‐216a‐3p presents a novel target of CRC treatment; rescuing miR‐216a‐3p expression in CRC might be a promising strategy for CRC treatment.