LncRNA SPRY4-IT1 is upregulated and promotes the proliferation of prostate cancer cells under hypoxia in vitro

被引:2
作者
Sang, Weicong [1 ]
Zhu, Rujian [1 ]
Liu, Dong [1 ]
Gong, Min [1 ]
机构
[1] Fudan Univ, Shanghai Pudong Hosp, Dept Urol, Pudong Med Ctr, 2800 Gongwei Rd, Shanghai 201399, Peoples R China
基金
中国国家自然科学基金;
关键词
long noncoding RNA; SPRY4-IT1; prostate cancer; hypoxia; S phase; LONG NONCODING RNAS; APOPTOSIS;
D O I
10.3892/ol.2023.13724
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The incidence and mortality rate of prostate cancer are among the highest for all cancers worldwide; this disease has a high cancer mortality rate in males, following lung cancer. Sprouty4-intron 1 (SPRY4-IT1) has been shown to play a variety of roles in tumors. Our previous study demonstrated that SPRY4-IT1 sponges microRNA-101-3p to promote the proliferation and metastasis of bladder cancer cells by upregulating enhancer of zeste homolog 2 expression; however, the role of SPRY4-IT1 in prostate cancer has not been fully established. In the present study, the expression levels, effects and mechanism of action of SPRY4-IT1 were investigated in prostate cancer tissues and cell lines using reverse transcription-quantitative PCR, western blotting, Cell Counting Kit-8 and flow cytometry assays. The results indicated that SPRY4-IT1 expression was upregulated in prostate cancer tissues and cell lines. Furthermore, hypoxia increased the expression levels of SPRY4-IT1 in prostate cancer cells. Knockdown of SPRY4-IT1 expression led to S-phase arrest, decreased expression levels of the cell cycle-associated proteins CDK2 and cyclin D1. AKT phosphorylation was also reduced by SPRY4-IT1 knockdown. In summary, the findings indicate the elevation of SPRY4-IT1 expression in prostate cancer. Under hypoxic conditions in vitro, SPRY4-IT1 overexpression promoted prostate cancer cell proliferation via a mechanism involving regulation of the cell cycle and the PI3K/AKT signaling pathway. Therefore, it may provide a basis for the development of targeted therapies.
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页数:8
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