Open AccessUpregulation of contactin‑1 expression promotes prostate cancer progression
Author(s) -
Boren Wang,
Xi Yang,
Ting Zhao,
Hanghang Du,
Tong Wang,
Suping Zhong,
Bo Yang,
Hui Li
Publication year - 2019
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2019.11244
Subject(s) - prostate cancer , cancer , cancer research , downregulation and upregulation , oncogene , metastasis , gene silencing , gene knockdown , epithelial–mesenchymal transition , prostate , vimentin , cancer cell , medicine , pi3k/akt/mtor pathway , tumor progression , protein kinase b , biology , cell cycle , signal transduction , apoptosis , immunohistochemistry , microbiology and biotechnology , biochemistry , gene
Contactin-1 (CNTN-1) has been reported to serve an oncogenic role in several cancer types. However, detailed mechanisms describing the influence of CNTN-1 in prostate cancer progression have not yet been elucidated. The present study aimed to determine the clinical significance of CNTN-1 expression in prostate cancer progression, and also to investigate the regulatory role of CNTN-1 in the proliferation, migration and invasive ability of prostate cancer cells. The results of the present study indicated that expression levels of CNTN-1 were significantly higher in prostate cancer tissues compared with adjacent normal tissues. Moreover, a high expression level of CNTN-1 was positively correlated with tumor size, stage and metastasis, as well as a poorer prognosis in patients with prostate cancer. Furthermore, CNTN-1-knockdown in prostate cancer cells (using short hairpin RNA) resulted in the significant inhibition of cancer cell proliferation, colony formation, migration and invasiveness. Silencing of CNTN-1 expression also suppressed epithelial-mesenchymal transition in prostate cancer cells via the upregulation of E-cadherin, and the downregulation of N-cadherin and vimentin expression. Inhibition of CNTN-1 expression also reduced the activity of the PI3K/AKT signaling pathway in prostate cancer cells. Thus, it was demonstrated that CNTN-1 expression is upregulated, and plays an oncogenic role, in prostate cancer cells. The results of the current study suggest that CNTN-1 may represent a promising therapeutic target, potentially improving the treatment of patients with prostate cancer.