HOXC13-AS accelerates cell proliferation and migration in oral squamous cell carcinoma via miR-378g/HOXC13 axis

•HOXC13-AS was upregulated in OSCC and silencing HOXC13-AS inhibited proliferation, migration, and EMT in OSCC cells.•HOXC13-AS post-transcriptionally upregulated HOXC13 in OSCC cells.•HOXC13-AS mediated malignant phenotypes in OSCC cells through targeting HOXC13.•HOXC13-AS induced HOXC13 expression...

Full description

Saved in:
Bibliographic Details
Published in:Oral oncology Vol. 111; p. 104946
Main Authors: Li, Wenlu, Zhu, Qiuyu, Zhang, Sanke, Liu, Lei, Zhang, Han, Zhu, Dandan
Format: Journal Article
Language:English
Published: England Elsevier Ltd 01-12-2020
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:•HOXC13-AS was upregulated in OSCC and silencing HOXC13-AS inhibited proliferation, migration, and EMT in OSCC cells.•HOXC13-AS post-transcriptionally upregulated HOXC13 in OSCC cells.•HOXC13-AS mediated malignant phenotypes in OSCC cells through targeting HOXC13.•HOXC13-AS induced HOXC13 expression by absorbing miR-378g. Oral squamous cell carcinoma (OSCC) is an aggressive cancer type in head and neck. A number of long non-coding RNAs (lncRNAs) are discovered to serve regulatory roles in OSCC. HOXC13 antisense RNA (HOXC13-AS) has been proved to behave as a tumor-facilitator in nasopharyngeal carcinoma, but its regulatory role in OSCC has never been investigated. In this study, GEPIA indicated that HOXC13-AS and its neighbor gene HOXC13 were upregulated in HNSC samples, and we consistently unveiled their upregulation in OSCC tissues and cell lines. Silencing HOXC13-AS abrogated OSCC cell proliferation, migration, and epithelial-to-mesenchymal transition (EMT). Moreover, HOXC13 overexpression rescued the influences of HOXC13-AS silence on OSCC cellular processes and in vivo tumor growth. Mechanistically, HOXC13-AS upregulated HOXC13 expression in OSCC through sequestering miR-378g, which was proved to exert suppressive functions in the malignant behaviors of OSCC cells. Further, HOXC13 was revealed to be positively correlated with HOXC13-AS and negatively with miR-378g in expression in OSCC samples. In sum, our findings suggested that HOXC13-AS functioned as a ceRNA to accelerate the malignant behaviors of OSCC cells via miR-378g/HOXC13 axis, shedding a new light on the lncRNA-targeted treatment for OSCC.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1368-8375
1879-0593
DOI:10.1016/j.oraloncology.2020.104946