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Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 193523, 9 pages
Research Article

PELP1 Suppression Inhibits Colorectal Cancer through c-Src Downregulation

1Hubei Province Key Laboratory on Cardiovascular, Cerebrovascular, and Metabolic Disorders, Hubei University of Science and Technology, Xianning 437100, China
2The Basic Medical School, Hubei University of Science and Technology, Xianning 437100, China
3School of Pharmacy, Hubei University of Science and Technology, Xianning 437100, China
4Wuhan Blood Center, Wuhan 430030, China

Received 13 February 2014; Accepted 20 April 2014; Published 22 May 2014

Academic Editor: Xiaoqian Chen

Copyright © 2014 Zhifeng Ning et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Proline-, glutamic acid-, and leucine-rich protein 1 (PELP1), a coregulator of estrogen receptors alpha and beta, is a potential protooncogene implicated in several human cancers, including sexual hormone-responsive or sexual hormone-nonresponsive cancers. However, the functions of PELP1 in colorectal cancer remain unclear. In this study, western blot and bioinformatics revealed that PELP1 expression was higher in several colorectal cancer cell lines than in immortalized normal colorectal epithelium. PELP1 silencing by short hairpin RNA promoted the senescence and inhibited the proliferation, colony formation, migration, invasion, and xenograft tumor formation of the CRC cell line HT-29. Moreover, PELP1 silencing was accompanied by c-Src downregulation. c-Src upregulation partly alleviated the damage in HT-29 malignant behavior induced by PELP1 RNA interference. In conclusion, PELP1 exhibits an oncogenic function in colorectal cancer through c-Src upregulation.