High C-X-C motif chemokine 5 expression is associated with malignant phenotypes of prostate cancer cells via autocrine and paracrine pathways

Qi,Yaling; Zhao,Wenjie; Li,Mengsen; Shao,Mingliang; Wang,Jingtao; Sui,Hongyu; Yu,Haibo; Shao,Wenwu; Gui,Shiliang; Li,Jing; Jia,Xiuyue; Jiang,Dali; Li,Yue; Zhang,Pengxia; Wang,Shuqiu; Wang,Weiqun

doi:10.3892/ijo.2018.4388

High C-X-C motif chemokine 5 expression is associated with malignant phenotypes of prostate cancer cells via autocrine and paracrine pathways

Authors:
- Yaling Qi
- Wenjie Zhao
- Mengsen Li
- Mingliang Shao
- Jingtao Wang
- Hongyu Sui
- Haibo Yu
- Wenwu Shao
- Shiliang Gui
- Jing Li
- Xiuyue Jia
- Dali Jiang
- Yue Li
- Pengxia Zhang
- Shuqiu Wang
- Weiqun Wang
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Affiliations: Department of Physiology, Basic Medical College, Jiamusi University, Jiamusi, Heilongjiang 154007, P.R. China, Affiliated Hospital, Hainan Medical College, Haikou, Hainan 570102, P.R. China, Department of Histology and Embryology, Basic Medicine and Life Science College, Hainan Medical College, Haikou, Hainan 571199, P.R. China, Department of Interventional Medicine, The Fifth Hospital, Shijiazhuang, Hebei 050000, P.R. China, Clinical Medical College, Jiamusi University, Jiamusi, Heilongjiang 154007, P.R. China
Published online on: April 30, 2018 https://doi.org/10.3892/ijo.2018.4388
Pages: 358-370

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Abstract

The present study aimed to examine the effects and mechanisms of exogenous C-X-C motif chemokine 5 (CXCL5) and lentiviral CXCL5 overexpression on the regulation of malignant behaviors of prostate cancer cells in vitro and in a nude mouse xenograft model. The expression levels of CXCL5 and a number of tumor-related genes were assessed by using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR), western blotting, ELISA, or immunohistochemistry in normal and cancerous prostate cells and tissues. Cell proliferation, colony formation, and Transwell assays were performed to determine the effects of exogenous, autocrine, and paracrine CXCL5 on prostate cancer cell proliferative and migratory capacity. The results indicated that CXCL5 expression was upregulated in PC‑3 and DU145 prostate cancer cells, in WPMY‑1 normal prostate stromal cells, and in RWPE‑1 prostate epithelial cells, as well as in prostate cancer tissue specimens. Exogenous CXCL5 exposure resulted in increase in prostate cancer cell proliferation, colony formation, and migration. In cells transfected with a CXCL5 overexpression vector, in cells cultured in conditioned medium from CXCL5-overexpressing WPMY cells, and in cells co-cultured with CXCL5‑OE WPMY cells prostate cancer cell malignant phenotypes were induced in an autocrine/paracrine fashion in vitro; similar results were observed in nude mouse xenografts. CXCL5 overexpression also regulated expression of tumor-related genes, including BAX, N-Myc downstream-regulated gene 3, extracellular signal-regulated kinase 1/2, C-X-C chemokine receptor type 2, interleukin 18, Bcl‑2, and caspase‑3. These data demonstrated that CXCL5 expression was upregulated in prostate cancer tissues and that exogenous CXCL5 protein exposure or CXCL5 overexpression promoted malignant phenotypes of prostate cancer cells in vitro and in vivo.

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