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The IκB family member Bcl-3 stabilizes c-Myc in colorectal cancer Free
Zhanjie Liu1,†, Yuhang Jiang1,†, Yinyong Hou2,†, Yiming Hu1, Xinwei Cao1, Yu Tao1, Chen Xu2, Sanhong Liu1, Shouli Wang1,3, Lunshan Wang1, Yufang Shi1, Ulrich Siebenlist4, and Xiaoren Zhang1,*
1Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai 200031, China
2Department of Pathology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, China
3Department of Pathology, Soochow University School of Medicine, Suzhou 215123, China
4Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
*Correspondence to:Xiaoren Zhang, E-mail: xrzhang@sibs.ac.cn
J Mol Cell Biol, Volume 5, Issue 4, August 2013, 280-282,  https://doi.org/10.1093/jmcb/mjt020

The proto-oncogene c-myc has been thought to play a critical role during the tumor-initiating process in multiple human cancers. Among others, colorectal cancer (CRC) is particularly associated with deregulated expression of c-Myc (Meyer and Penn, 2008; Wilkins and Sansom, 2008). Physiologically, Myc mRNA and protein levels are tightly regulated, and the Myc protein is highly unstable. The high levels of Myc protein in human CRC could be attributed to the altered Myc turnover and aberrant transcriptional activation of the myc genes (Ikegaki et al., 1986; Welcker and Clurman, 2008).


Volume 5, Issue 4
August 2013