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IL‐17F facilitates prostate cancer cell malignant phenotypes via activation of the PI3K/AKT signalling pathway
Author(s) -
Zhu Xu,
Zhao Shuli,
Ma Xingxin,
Cao Zhigang
Publication year - 2020
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.13750
Subject(s) - pi3k/akt/mtor pathway , protein kinase b , cancer research , viability assay , ly294002 , cell growth , prostate cancer , cell , biology , signal transduction , downregulation and upregulation , cell migration , cancer , microbiology and biotechnology , medicine , gene , biochemistry
Prostate cancer (PCa) is known as one of the most common cancers in men all over the world. Previous studies have identified that the pro‐inflammatory mediator interleukin‐17F (IL‐17F) aggravates the progression of several diseases. However, whether IL‐17F plays a role in PCa is still lack of enough exploration. In this study, IL‐17F expression was strikingly upregulated in PCa tissues. Treatment of IL‐17F promoted cell viability at a dose‐dependent manner. Further, functional assays were implemented by treatment of 100 ng/ml of IL‐17F. Cell viability, proliferation, migration, invasion and stemness were promoted by 100 ng/ml of IL‐17F. IL‐17F increased the expression of p‐PI3K and p‐AKT in PCa cells, indicating that IL‐17F might activate the PI3K/AKT signalling pathway in PCa cells. LY294002 (the inhibitor of the PI3K/AKT signalling pathway) could reverse the facilitating effects of IL‐17F treatment on PCa cell viability, proliferation, migration, invasion and stemness. Taken together, current study revealed that IL‐17F facilitated PCa cell malignant phenotypes via activation of the PI3K/AKT signalling pathway, offering a potential therapeutic target for PCa.