Expression And Significance Of BNIP3L In Prostate Cancer

Objective:To study the expression and significance of BNIP3L in prostate cancer developmentMethods:(1) Prostate cancer tissues and normal prostate tissues were collected and the expression of BNIP3L was by immunohistochemical staining. The relation beween BNIP3L expression and clinical pathological characteristics of prostate cancer were analyzed.(2) Expression of BNIP3L in different prostate cancer cell line were detected. Vectors carrying either overexpress BNIP3L or BNIP3L shRNA were constructed and transfected to LNCap anc C4-2 cells in the condition with or without serum androgen deprivation. Their effects on cell proliferation,cell cycle, apoptosis, and colony formation were analyzed.(3) After manipulation of BNIP3L in PCa cells, migration and invasion ability of PCa cells were evaulated using Transwell assay expression of EMT related genes were determined.Results:(1) BNIP3L mainly located in cytoplasm of PCa cells.PCa tissues had a higher expression of BNIP3L than normal prostate. Higher expression of BNIP3L is correlated with PSA level, Gleason score, TNM staging, AR,distant metastasis,CRPC and reduced total survival rate.(2) There was no expression of BNIP3L in normal prostate cells, while expression of BNIP3L is high in prostate cancer cell lines.(3)Overexpression of BNIP3L could promote cell growth, inhibt apoptosis, and promote cell cycle progression,(4) Overexpression of BNIP3L can promote migration and invasion of PCa cells; which maybe go through up-regulating the expression of EMT-related genes include N-Cadhein, Vimentin, Slug, Twist and Snail, while inhibited the epithelial marker E-Cadherin.Conclusions:(1) BNIP3L is overexpressed in prostate cancer tissue, and is closely related to the occurrence, development and progression of prostate cancer;(2) BNIP3L is overexpressed in prostate cancer cell lines, but not expressed in normal prostate cells.(3) BNIP3L promote cell growth, cell cycle, and inhibit apoptosis in prostate cancer.(4) BNIP3L promote PCa metastasis via regulation of EMT related genes.