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Long noncoding RNA SNHG12 modulated by human papillomavirus 16 E6/E7 promotes cervical cancer progression via ERK/Slug pathway
Author(s) -
Lai ShuYu,
Guan HongMei,
Liu Jie,
Huang LiJun,
Hu XiaoLin,
Chen YiHong,
Wu YiHua,
Wang Ying,
Yang Qi,
Zhou JueYu
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29446
Subject(s) - slug , gene knockdown , carcinogenesis , cancer research , long non coding rna , biology , epithelial–mesenchymal transition , mapk/erk pathway , phenotype , metastasis , rna , signal transduction , apoptosis , microbiology and biotechnology , cancer , gene , genetics
Recently, long noncoding RNA SNHG12 has been reported to be dysregulated in various types of cancer. This study investigated its biological function and the underlying molecular mechanism in cervical squamous cell carcinoma (CSCC). We found that SNHG12 was significantly overexpressed in CSCC tissues. Further evidence showed that human papillomavirus (HPV) type 16 E6 and E7 might regulate the expression level of SNHG12 by modulating transcription factor c‐Myc. Functional experiments suggested that SNHG12 knockdown dramatically repressed CSCC cells proliferation, migration, and invasion while induced apoptosis in vitro as well as suppressed tumor growth in vivo. In addition, SNHG12 could facilitate epithelial–mesenchymal transition through ERK/Slug/E‐cadherin pathway at least in part. Our findings highlight SNHG12 functions as an oncogenic long noncoding RNA in malignant phenotype and tumorigenesis of CSCC, which implicate it may be a potential target for CSCC treatment.