DLX1, a binding protein of beta-catenin, promoted the growth and migration of prostate cancer cells

• Published in: Experimental cell research Vol. 363; no. 1; pp. 26 - 32
• Main Authors: Liang, Ming, Sun, Yan, Yang, Huai-Liang, Zhang, Bin, Wen, Ji, Shi, Ben-Kang
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.02.2018
• Subjects: 60 APPLIED LIFE SCIENCES; beta Catenin - metabolism; Beta-catenin/TCF signaling; Cell growth and migration; Cell Line, Tumor; Cell Movement - physiology; Cell Proliferation - physiology; COLONY FORMATION; DLX1; Gene Expression Regulation, Neoplastic - genetics; Homeodomain Proteins - metabolism; Humans; Male; NEOPLASMS; PROSTATE; Prostate - metabolism; Prostate cancer; Prostatic Neoplasms - metabolism; Transcription Factors - metabolism; Up-Regulation; Beta-catenin/TCF signaling; DLX1; Prostate cancer; Cell growth and migration
• ISSN: 0014-4827; 1090-2422
• DOI: 10.1016/j.yexcr.2018.01.007

Several studies have indicated the involvement of DLX1 in the progression of prostate cancer. However, the functions of DLX1 in the prostate cancer and the underlying molecular mechanism remains largely unknown. In this study, we have shown that DLX1 was up-regulated in the prostate clinical samples. DLX1 promoted the growth, migration and colony formation of prostate cancer cells by activating beta-catenin/TCF signaling. DLX1 interacted with beta-catenin and enhanced the interaction between beta-catenin and TCF4. Taken together, this study demonstrated that DLX1 exerted the oncogenic roles on the prostate cancer by activating beta-catenin/TCF signaling.