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microRNA‐802 inhibits cell proliferation and induces apoptosis in human cervical cancer by targeting serine/arginine‐rich splicing factor 9
Author(s) -
Zhang Qianwen,
Lv Rui,
Guo Wenjia,
Li Xiaoning
Publication year - 2019
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.28321
Subject(s) - microrna , cancer research , transfection , cell cycle , cancer , cervical cancer , apoptosis , cell growth , cancer cell , biology , cell culture , medicine , gene , genetics
microRNAs (miRNAs) play crucial roles in cancer development and progression by targeting mRNAs for degradation and/or translational repression. microRNA‐802 (miR‐802) has been reported as a tumor suppressor and its deregulation is observed in various human cancers. However, the prognostic value of miR‐802 and its underlying mechanisms involved in human cervical cancer are poorly investigated. The purposes of this study were to explore the role of miR‐802 in cervical cancer and to clarify the regulation of serine/arginine‐rich splicing factor 9 (SRSF9) by miR‐802. Here, we found that miR‐802 was downregulated in both cervical cancer tissues and cell lines. Transfection of a miR‐802 mimic into cervical cancer cells inhibited their proliferation and colony formation, and promoted cell cycle arrest at the G0/G1 phase and cell apoptosis. In addition, we found that miR‐802 could directly target the 3′‐untranslated region of SRSF9 and suppress SRSF9 expression. Rescue experiments revealed that overexpression of SRSF9 partially reversed the inhibition effect of miR‐802 in cervical cancer cells. Overall, these findings demonstrate that miR‐802 functions as a tumor suppressor in cervical cancer by targeting SRSF9, suggesting that miR‐802 might serve as a potential therapeutic target in cervical cancer.