Gang Liu*, Jingjun Zhang*, Mingyong Liu, Zhiqiang Sun, Hanwen Cui
Department of Urology, Tianjin Fifth Central Hospital, Tianjin, China.
*Gang Liu and Jingjun Zhang contributed equally to this work.
Summary
Purpose: To investigate the expression characteristics of LncARSR in prostate cancer tissues and further explore the specific mechanism by which LncARSR promotes the proliferation of prostate cancer (PCa) cells.
Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to examine LncARSR expression in 50 pairs of PCa tumor tissues and adjacent normal ones, and the relationship between LncARSR and clinicopathologic indicators or prognosis of these PCa cases were also analyzed. Meanwhile, qRT-PCR further verified LncARSR expression in PCa cell lines. LncARSR knockdown models were constructed in PCa cell lines 22RV1 and PC-3. The impacts of LncARSR on the function of PCa cells were assessed by cell counting kit-8 (CCK-8), plate cloning experiments, and 5-Ethynyl-2’- deoxyuridine (EdU) assay. Finally, the relationship between LncARSR and PTEN / PI3K / AKT pathway was analyzed by Western blotting.
Results: Our data showed that LncARSR expression in PCa tumor specimens was remarkably higher than in adjacent ones. In comparison to patients in group of low LncARSR expression, patients in high expression group showed higher pathologic grade, larger tumor size, and lower overall survival. In vitro cell experiments suggested that knockdown of LncARSR significantly suppressed the proliferative capacity of PCa cells, enhanced the expression of the key protein PTEN in the PTEN / PI3K / AKT signaling, while reduced the other proteins such as p-PI3K, p-AKT, and p-mTOR. In addition, silencing PTEN reversed the inhibitory effect of knockdown of LncARSR on the proliferation of PCa cells.
Conclusions: LncARSR, highly expressed in PCa tissues and cell lines, is remarkably associated with pathologic stage, tumor size, and poor prognosis of patients with PCa. In addition, LncARSR may promote the malignant progression of PCa through activating the PTEN / PI3K / AKT signaling pathway.
Key words: LncARSR, PTEN / PI3K / AKT, prostate cancer, malignant progression.
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