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Vinculin orchestrates prostate cancer progression by regulating tumor cell invasion, migration, and proliferation
Author(s) -
Zheng Xiaonan,
Xu Hang,
Gong Lina,
Cao Dehong,
Jin Tao,
Wang Yan,
Pi Jinkui,
Yang Yang,
Yi Xianyanling,
Liao Dazhou,
Jin Xi,
Wei Qiang,
Yang Lu,
Li Hong,
Ai Jianzhong
Publication year - 2021
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.24113
Subject(s) - gene knockdown , cancer research , cell growth , viability assay , in vivo , biology , cell migration , downregulation and upregulation , microbiology and biotechnology , tumor progression , cell , prostate cancer , methylation , cell culture , cancer , biochemistry , gene , genetics
Background Prostate cancer (PCa) is a leading cause of death in men, and effective treatment of PCa requires further development. Our study aimed to investigate the potential role of vinculin (VCL) in PCa progression in vitro and in vivo. Methods We investigated the methylation level of the VCL promoter based on the TCGA database. The knockdown efficacy of VCL gene expression was confirmed by quantitative polymerase chain reaction, Western blot analysis, and immunofluorescence. Furthermore, morphological changes in PCa cells were detected using phalloidin staining. The mobility of PCa cells was measured using transwell assays and high‐content analysis. Moreover, cell growth and viability were determined using the colony formation and cell counting kit‐8 assays. The role of VCL in tumor growth in vivo was investigated using a subcutaneous xenograft model generated by injecting tumor cells into the right flank of BALB/c nude mice. Results The methylation level of the VCL promoter in PCa was significantly downregulated concomitant with age and the progression of nodal metastasis. VCL expression was markedly decreased by shRNA. Importantly, VCL knockdown significantly changed the cell morphology; inhibited the migration, invasion, and movement; and repressed colony formation and viability of PCa cells in vitro. Furthermore, downregulation of VCL suppressed tumor growth in vivo. Conclusions Our study comprehensively evaluated the role of VCL in PCa progression in vivo and in vitro. The findings of the present study suggest that VCL can be a potential target for PCa prognosis and treatment.