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Repression of HIP/RPL29 expression induces differentiation in colon cancer cells
Author(s) -
Liu JianJun,
Huang Bao Hua,
Zhang Jinqiu,
Carson Daniel D.,
Hooi Shing Chuan
Publication year - 2006
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.20589
Subject(s) - psychological repression , colorectal cancer , cancer research , microbiology and biotechnology , expression (computer science) , chemistry , cancer , gene expression , medicine , biology , gene , biochemistry , computer science , programming language
We had previously shown that the expression of heparin/heparan sulfate interacting protein/ribosomal protein L29 (HIP/RPL29) was upregulated in colon cancer tissues. The present study investigated the role of HIP/RPL29 in differentiation in colon cancer cells. Inducing cellular differentiation in HT‐29 cells by both sodium butyrate and glucose deprivation resulted in a significant downregulation of HIP/RPL29 expression. The β‐catenin/Tcf‐4 pathway is the most important pathway controlling the switch between cellular differentiation and proliferation in intestinal epithelial cells. Inducing differentiation by dominant‐negative inhibition of the β‐catenin/Tcf‐4 complexes in LS174T cells also resulted in downregulation of HIP/RPL29. To determine whether a lower expression of HIP/RPL29 could induce differentiation in cancer cells, small interfering RNA (siRNA) targeting HIP/RPL29 was transfected into LS174T cells. The resultant knockdown of HIP/RPL29 expression induced cellular differentiation, as shown by the increased expression of two known markers of differentiation in LS174T cells, galectin‐4 and mucin‐2. In addition, the differentiation process induced by repression of HIP/RPL29 expression was accompanied by the upregulation of p21 and p53. In conclusion, HIP/RPL29 plays a role in the cellular differentiation process in colon cancer cells. The differentiation process is at least partially mediated by the upregulation of p21 and p53 pathways. J. Cell. Physiol. 207: 287–292, 2006. © 2006 Wiley‐Liss, Inc.