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LINC00116 enhances cervical cancer tumorigenesis through miR‐106a/c‐Jun pathway
Author(s) -
Lai Yiqing,
Zhou Beibei,
Tan Qingqing,
Xu Juan,
Wan Ting,
Zhang Lina
Publication year - 2020
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.29447
Subject(s) - carcinogenesis , hela , gene knockdown , cancer research , mtt assay , cervical cancer , cancer , western blot , cell growth , biology , cell , cell culture , gene , genetics
Some studies imply that LINC00116 is involved in cervical cancer progression; however, the molecular mechanism by which LINC00116 modulating tumorigenesis of cervical cancer remains not clear. Reverse transcription‐quantitative PCR (RT‐qPCR) and the Western blot approaches were employed to probe genes expression levels. To examine the tumorigenic abilities of cervical cancer cells, MTT assay, Transwell assay, and wound‐healing assay were used to investigate proliferation, invasion, and migration of HeLa or C‐33A cells. LINC00116 knockdown attenuates cell proliferation, invasion, and migration of cervical cancer cells. miR‐106a directly binds LINC00116 and regulate each other. Moreover, miR‐106a inhibitor remarkably enhanced tumorigenesis of shLINC00116 HeLa cells. Through bioinformatic and dual‐luciferase reporter assay, the results showed that miR‐106a mimic directly targeted and downregulated the c‐Jun. c‐Jun overexpression could greatly rescue miR‐106a mimic‐modulated cervical cancer tumorigenesis. LINC00116 knockdown and miR‐106a mimic‐modulated programmed cell death ligand 1 (PD‐L1) expression, which could be reverted by c‐Jun introduction. LINC00116, PD‐L1, and JUN were both upregulated in cervical cancer tumors compared to normal tissues. Lower expression levels of LINC00116 and JUN, as well as higher level of miR‐106a were closely associated with higher overall survival of cervical cancer patients. Here, we report a novel role for LINC00116 in tumorigenesis of cervical cancer by regulating miR‐106a/c‐Jun axis. Our findings provide a foundation for understanding cervical cancer and facilitate the development of therapeutical approaches by targeting LINC00116.