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Title

Upregulation of contactin-1 expression promotes prostate cancer progression.

Authors

Wang, Boren; Yang, Xi; Zhao, Ting; Du, Hanghang; Wang, Tong; Zhong, Suping; Yang, Bo; Li, Hui

Abstract

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.

Subjects

PROSTATE cancer; CANCER invasiveness; PROSTATE cancer prognosis; CASTRATION-resistant prostate cancer; CANCER cell proliferation; PROSTATE cancer patients

Publication

Oncology Letters, 2020, Vol 19, Issue 2, p1611

ISSN

1792-1074

Publication type

Academic Journal

DOI

10.3892/ol.2019.11244

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