The role of DEAD-box RNA helicase p68 (DDX5) in the development and treatment of breast cancer

Hojjat‐Farsangi, Mohammad and Hashemi, Vida and Masjedi, Ali and Hazhir‐karzar, Bita and Tanomand, Asghar and Sandoghchian Shotorbani, Siamak (2019) The role of DEAD-box RNA helicase p68 (DDX5) in the development and treatment of breast cancer. Journal of Cellular Physiology, 234. pp. 5478-5487.

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RNA helicase p68 or DEAD (Asp-Glu-Ala-Asp) box polypeptide 5 (DDX5) is a unique member of the highly conserved protein family, which is involved in a broad spectrum of biological processes, including transcription, translation, precursor messenger RNA processing or alternative splicing, and microRNA (miRNA) processing. It has been shown that p68 is necessary for cell growth and participates in the early development and maturation of some organs. Interestingly, p68 is a transcriptional coactivator of numerous oncogenic transcription factors, including nuclear factor-κβ (NF-κβ), estrogen receptor α (ERα), β-catenin, androgen receptor, Notch transcriptional activation complex, p53 and signal transducer, and activator of transcription 3 (STAT3). Recent studies on the role of p68 (DDX5) in multiple dysregulated cellular processes in various cancers and its abnormal expression indicate the importance of this factor in tumor development. Discussion of the precise role of p68 in cancer is complex and depends on the cellular microenvironment and interacting factors. In terms of the deregulated expression of p68 in breast cancer and the high prevalence of this cancer among women, it can be informative to review the precise function of this factor in the breast cancer. Therefore, an attempt will be made in this review to clarify the tumorigenic function of p68 in association with its targeting potential for the treatment of breast cancer.

Item Type: Article
Subjects: QW Microbiology and Immunology
Divisions: Faculty of Medicin > Department of Microbiology
Depositing User: محسن زارعی
Date Deposited: 17 Apr 2019 07:56
Last Modified: 17 Apr 2019 07:56

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