Background: Cervical cancer is one of the most common gynecologic tumors. Evidence is accumulating that long non-coding RNAs participate in the pathogenesis of cancers, but the expression and role of lncRNA LINC00313 in cervical carcinoma is not reported.
Methods: We measured the expression levels of LINC00313 in clinical samples of cervical carcinoma and investigated the function of LINC00313 in the regulation of proliferation, metastasis, and EMT. Luciferase reporter assay was employed to explore the molecular regulation process of LINC00313.
Results: Our data showed that the levels of LINC00313 in cervical carcinoma tissues and cells were significantly up-regulated. Functionally, LINC00313 accelerated the progression, migration, and EMT of SiHa and Hela cells. Luciferase reporter assay confirmed that miR-4677-3p/CDK6 regulatory axis is the direct downstream of LINC00313. Functional gain- and loss-of-function strategies further showed that LINC00313 induced the up-regulation of CDK6 expression through competitive binding with miR-4677-3p, leading to promote the progression of cervical carcinoma.
Conclusion: Our results demonstrated that LINC00313 accelerated the progression of cervical cancer through the miR-4677-3p/CDK6 regulatory axis. LncRNA LINC00313 may serve as a potential target for the diagnosis and treatment of cervical carcinoma.
Keywords: cervical carcinoma, LINC00313, miR-4677-3p, CDK6