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

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...

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Bibliographic Details
Published in:Experimental cell research 2018-02, Vol.363 (1), p.26-32
Main Authors: Liang, Ming, Sun, Yan, Yang, Huai-Liang, Zhang, Bin, Wen, Ji, Shi, Ben-Kang
Format: Article
Language:English
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
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Summary: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.
ISSN:0014-4827
1090-2422
DOI:10.1016/j.yexcr.2018.01.007