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...
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Published in: | Oral oncology Vol. 111; p. 104946 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
Elsevier Ltd
01-12-2020
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Subjects: | |
Online Access: | Get full text |
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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. |
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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 |