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New Insights into the PTB-Associated Splicing Factor (PSF) and Peroxisome Proliferator Activated Receptor gamma (PPARγ) in Colorectal Carcinogenesis | Abstract
ISSN: 1948-5956

Journal of Cancer Science & Therapy
Open Access

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Review Article

New Insights into the PTB-Associated Splicing Factor (PSF) and Peroxisome Proliferator Activated Receptor gamma (PPARγ) in Colorectal Carcinogenesis

Tamotsu Tsukahara1, Yoshikazu Matsuda2 and Hisao Haniu3*
1Department of Molecular and Cellular Physiology, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan
2Clinical Pharmacology Educational Center, Nihon Pharmaceutical University, Ina-machi, Saitama, 362-0806, Japan
3Department of Orthopaedic Surgery, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan
Corresponding Author : Tamotsu Tsukahara
Department of Molecular and Cellular Physiology
Shinshu University School of Medicine
3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan
E-mail: [email protected]
Received May 02, 2013; Accepted May 22, 2013; Published May 25, 2013
Citation: Tsukahara T, Matsuda Y, Haniu H (2013) New Insights into the PTBAssociated Splicing Factor (PSF) and Peroxisome Proliferator-Activated Receptor gamma (PPARγ) in Colorectal Carcinogenesis. J Cancer Sci Ther 5:209-211. doi:10.4172/1948-5956.1000208
Copyright: © 2013 Tsukahara T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

PTB-associated Splicing Factor (PSF) is a multifunctional protein involved in transcription repression, premRNA processing, and DNA repair. Transcriptional repression by PSF is mediated by its interaction with nuclear hormone receptors. However, the physiological context of PSF in regard to nuclear receptor signaling is still unclear. In this review, our recent study identified PSF as a novel PPARγ-interacting protein and demonstrated that PSF is involved in several important regulatory steps of colon cancer cell proliferation. Recently, the aberrant expression of PSF in tumor cells has been implicated in resistance to drugs that are commonly used in cancer therapy. Therefore, it might be possible to develop and to optimize drugs that inhibit PSF and correct abnormal splicing, resulting in enhanced tumor cell migration, invasion, and proliferation. In this review, we summarize current understanding of the mechanisms underlying the PSF-PPARγ axis and its role in the control of colorectal carcinogenesis.

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