Abrogation of Gli3 expression suppresses the growth of colon cancer cells via activation of p53

• Published in: Experimental cell research 2012-03, Vol.318 (5), p.539-549
• Main Authors: Kang, Han Na, Oh, Sang Cheul, Kim, Jun Suk, Yoo, Young A.
• Format: Article
• Language: English
• Subjects: 60 APPLIED LIFE SCIENCES; Antibodies, Monoclonal, Humanized - pharmacology; Antineoplastic Agents - pharmacology; Bevacizumab; Cancer; Cell Line, Tumor; CELL PROLIFERATION; Cell Proliferation - drug effects; Cells; Colon; Colon cancer; Colonic Neoplasms; Fluorouracil - pharmacology; Gene Expression; Gene Knockdown Techniques; Gli; Hedgehog Proteins - metabolism; Humans; INHIBITION; Kruppel-Like Transcription Factors - genetics; Kruppel-Like Transcription Factors - metabolism; LARGE INTESTINE; MDM2; MESSENGER-RNA; NEOPLASMS; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - metabolism; p53; Protein Stability; PROTEINS; Proteolysis; Proto-Oncogene Proteins c-mdm2 - metabolism; Ribonucleic acid; RNA; RNA Interference; Signal Transduction; Sonic hedgehog (Shh); Tumor Suppressor Protein p53 - genetics; Tumor Suppressor Protein p53 - metabolism; Tumors; Ubiquitination; Zinc Finger Protein Gli3
• ISSN: 0014-4827; 1090-2422
• DOI: 10.1016/j.yexcr.2011.12.010

p53, the major human tumor suppressor, appears to be related to sonic hedgehog (Shh)–Gli-mediated tumorigenesis. However, the role of p53 in tumor progression by the Shh–Gli signaling pathway is poorly understood. Herein we investigated the critical regulation of Gli3–p53 in tumorigenesis of colon cancer cells and the molecular mechanisms underlying these effects. RT-PCR analysis indicated that the mRNA level of Shh and Gli3 in colon tumor tissues was significantly higher than corresponding normal tissues (P