Long non-coding RNA LSINCT5 promotes ovarian cancer cell proliferation, migration and invasion by disrupting the CXCL12/CXCR4 signalling axis
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- Published online on: March 12, 2018 https://doi.org/10.3892/ol.2018.8241
- Pages: 7200-7206
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Copyright: © Long et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Long stress-induced noncoding transcript 5 (LSINCT5) is a member of the LSINCT family, members of which are expressed during stress-induced cell formation and have also been reported to promote cancer progression. In the present study, the association between LSINCT5 expression and clinical significance was investigated and the biological function of LSINCT5 in epithelial ovarian cancer (EOC) was explored. LSINCT5 expression was examined in EOC tissues by reverse transcription‑quantitative polymerase chain reaction and its association with clinicopathological factors was analysed. Cell proliferation, migration and invasion tests were performed to observe the role of LSINCT5 in human ovarian cancer cell lines in vitro. The negative control (NC) and siLSINCT5 SKOV3 cells were treated with chemokine ligand 12 (CXCL12) and their proliferation, migration and invasion activities were examined. LSINCT5 was overexpressed in EOC compared with normal ovarian tissue. LSINCT5 expression was significantly associated with the International Federation of Gynecologists and Obstetricians cancer stage and the presence of lymphatic metastases. Silencing LSINCT5 significantly reduced the expression of chemokine receptor 4 (CXCR4) and inhibited SKOV3 cell proliferation, migration and invasion, however the CXCL12 expression level had no significant change. When NC and siLSINCT5‑SKOV3 cells were treated with CXCL12, the proliferation and invasion ability were significantly enhanced. The migration ability of the siLSINCT5‑SKOV3 cells was also significantly enhanced. The present study indicated that LSINCT5 serves an important role in ovarian cancer metastasis by regulating the CXCL12/CXCR4 signalling axis, suggesting that this pathway may be a potential target for the treatment of patients with EOC.