OBJECTIVE: To investigate the clinical functions and the detailed mechanism of long noncoding RNA (IncRNA) JPX in human ovarian cancer cell lines.
PATIENTS AND METHODS: The expression of JPX in ovarian cancer tissues and cell lines was detected by Real-time polymerase chain reaction (RT-PCR). The correlation between JPX expression and prognosis was analyzed by follow-up data. The OVCAR-3 cell proliferation, invasion and migration were measured by methyl thiazolyl tetrazolium (MTT) assay, cloning formation assay and scratch assay. The cell apoptosis was detected by Bcl-2, Bax, and Caspase-3 activity. PI3K/mTOR inhibitor treatment and Western blot proved that JPX functions associated with PI3K/Akt/mTOR signaling and test the protein levels of p-PI3K, p-Akt, p-mTOR.
RESULTS: RT-PCR results showed that the expression of JPX was upregulated in ovarian cancer tissues and ovarian cancer cell lines (p < 0.05), and it was significantly increased in large tumor tissues and metastatic lymph nodes (p < 0.05). The survival rate of high JPX expression patients was much lower than low JPX expression patients (p < 0.05), indicating that high expression of JPX predicted poor prognosis in patients with ovarian cancer. MTT assay, colony formation and scratch assay showed the repression of JPX and resulted with significantly decreased in cell proliferation, invasion and migration of OVCAR-3 cells compared with the control (p < 0.05). PI3K/mTOR inhibitor treatment showed overexpression of JPX could activate the PI3K/Akt/mTOR signaling pathway. Western blot assay showed that the expressions of p-PI3K, p-Akt, p-mTOR were significantly increased after overexpression of JPX (p < 0.05), and after the inhibition of PI3K/Akt/mTOR signaling pathway and overexpression of JPX, the tumor cell proliferation, invasion and migration were significantly repressed, compared with the control (p < 0.05).
CONCLUSIONS: JPX could predict the poor prognosis in patients with ovarian cancer, which could promote the tumor cell proliferation, invasion and migration in human ovarian cancer cell lines and inhibited the cell apoptosis through activating PI3K/Akt/mTOR signaling pathway.