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Authors Mu M, Li Y, Zhan Y, Li X, Zhang B
Received 18 May 2018
Accepted for publication 16 August 2018
Published 13 November 2018 Volume 2018:11 Pages 8033—8044
DOI https://doi.org/10.2147/OTT.S174637
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Cristina Weinberg
Peer reviewer comments 4
Editor who approved publication: Dr Leo Jen-Liang Su
Background: Oral
tongue squamous cell carcinoma (OTSCC) is an aggressive cancer which has high
mortality rates. HOXA transcript at the distal tip (HOTTIP) is a lncRNA that
can be used as a prognostic marker in multiple carcinomas. The expression of
HOTTIP is found to be elevated in OTSCC tissues, and such elevation is
correlated with poor prognosis. However, its functional role in regulating the
growth and metastasis of OTSCC cells remains elusive and requires further
investigation.
Methods: HOTTIP-silenced
OTSCC cells were established by inhibiting HOTTIP expression via its exclusive
shRNA. Whether HOTTIP knockdown affected the aggressive tumor behaviors of
OTSCC cells was investigated in vitro and in vivo.
Results: We found
that HOTTIP shRNA restrained the cell proliferation and arrested the cell cycle
at G1 phase in TSCCA and TCA8113 cells. The expression levels of cyclins B, D1,
and E were downregulated in HOTTIP-silenced cells. HOTTIP silencing suppressed
the growth of xenograft tumors. Moreover, the silencing of HOTTIP triggered
apoptosis in TSCCA and TCA8113 cells and altered the expression of a group of
apoptosis-related molecules: downregulated Bcl-2, upregulated Bax, and enhanced
the cleavage of caspase 3 and PARP. Knockdown of HOTTIP also suppressed the
migration, invasion, and epithelial–mesenchymal transition (EMT) of both TSCCA
and TCA8113 cell lines.
Conclusion: Our
findings suggest that HOTTIP is required by the OTSCC cells to maintain their
growth and metastasis in vitro. It may serve as a promising potential candidate
for OTSCC therapy.
Keywords: HOTTIP,
oral tongue squamous cell carcinoma, proliferation, metastasis, apoptosis,
tumorigenicity