LncRNA SPRY4‑IT1 is upregulated and promotes the proliferation of prostate cancer cells under hypoxia in vitro
- Weicong Sang
- Rujian Zhu
- Dong Liu
- Min Gong
Affiliations: Department of Urology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai 201399, P.R. China
- Published online on: February 17, 2023 https://doi.org/10.3892/ol.2023.13724
Copyright: © Sang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
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.