Premium
LncRNA NOC2L‐4.1 functions as a tumor oncogene in cervical cancer progression by regulating the miR‐630/YAP1 pathway
Author(s) -
Wang Qingwei,
Ding Jin,
Nan Guo,
Lyu Yuanyuan,
Ni Guantai
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.28949
Subject(s) - yap1 , hela , gene knockdown , cancer research , gene silencing , cell growth , oncogene , biology , microrna , long non coding rna , cell , downregulation and upregulation , cervical cancer , cell migration , cancer , microbiology and biotechnology , cell culture , transcription factor , cell cycle , gene , biochemistry , genetics
Long noncoding RNA (lncRNA) is a new class of noncoding RNA playing an indispensable role in different diseases by regulating miRNA. Our previous studies have suggested that miR‐630 was decreased in patients with cervical cancer. Recently, studies have shown that lncRNA NOC2L‐4.1 was abnormally expressed in patients with cervical cancer and can target miR‐630. Therefore, we wanted to identify the integrated relationship between lncRNA NOC2L‐4.1 and miR‐630 in the pathological processes regarding cervical cancer either in vitro or in vivo. Quantitative reverse transcription‐polymerase chain reaction detection shows that compared with human normal cervical epithelial cell, the expression of lncRNA NOC2L‐4.1 was significantly increased and the expression of miR‐630 was decreased in cell lines of cervical cancer. Moreover, luciferase reporter assay showed that miR‐630 was a target of lncRNA NOC2L‐4.1. The in vitro study found that downregulation of lncRNA NOC2L‐4.1 suppressed cervical cancer cell migration (transwell assays) and proliferation (cell counting kit‐8 and cloning formation assays). miR‐630 specific inhibitor treatment reversed the inhibitory effect of lncRNA NOC2L‐4.1 on cell proliferation and migration. Further studies also found that yes‐associated protein 1 (YAP1) was the target of miR‐630. Overexpression YAP1 suppressed miR‐630 overexpression induced cell proliferation and inhibition of migration. Tumors induced by implantation of lncRNA NOC2L‐4.1‐knockdown Hela cells in nude mice showed that lncRNA NOC2L‐4.1 silencing decreased the growth of tumors in both volume and weight by regulation of miR‐630/YAP1. Taken together, our study reveals the important role of lncRNA NOC2L‐4.1/miR‐630/YAP1 regulatory network in cervical cancer, which provides new insights concerning the pathogenesis of cervical cancer.