Cluster of differentiation 166 (CD166) regulates cluster of differentiation (CD44) via NF-κB in liver cancer cell line Bel-7402

Lifang Ma; Qiuhui Pan; Fenyong Sun; Yongchun Yu; Jiayi Wang

doi:10.1016/j.bbrc.2014.07.128

Cluster of differentiation 166 (CD166) regulates cluster of differentiation (CD44) via NF-κB in liver cancer cell line Bel-7402

Biochem Biophys Res Commun. 2014 Aug 22;451(2):334-8. doi: 10.1016/j.bbrc.2014.07.128. Epub 2014 Aug 2.

Authors

Lifang Ma¹, Qiuhui Pan², Fenyong Sun³, Yongchun Yu⁴, Jiayi Wang⁵

Affiliations

¹ Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, PR China. Electronic address: malifang0606118@126.com.
² Department of Central Laboratory, Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, PR China. Electronic address: panqiuhui123@126.com.
³ Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, PR China. Electronic address: sunfenyong@126.com.
⁴ Shanghai Municipal Hospital of Traditional Chinese Medicine Affiliated to Shanghai TCM University, Shanghai 200071, PR China. Electronic address: yueyongchun88@163.com.
⁵ Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, PR China. Electronic address: karajan2@163.com.

PMID: 25094049
DOI: 10.1016/j.bbrc.2014.07.128

Abstract

Cluster of differentiation 166 (CD166) is critical for liver cancer cell survival. Our previously study demonstrated that CD166 exerts its anti-apoptotic role through interaction with YAP in liver cancer. However, the interaction between CD166 and other cell surface molecules remains unclear in liver cancer cells. In the current study, we found that both mRNA and protein of CD44 expression was significantly inhibited by knocking-down CD166. Moreover, CD166 affected-CD44 expression is dependent of transcription via blocking NF-κB pathway. On the contrary, CD44 promoted up-regulation of CD166 mRNA and protein. And it may be through E3 ubiquitin ligases COP1 and UBC3 to regulate CD166 protein degradation. Collectively, these results suggest that CD166 and CD44 play important roles in liver cancer development. Therefore, CD166 may develop as a potential therapeutic molecule target for the treatment of liver cancer.

Keywords: COP1; Protein degradation; Signaling pathway; Transcription factor; UBC3.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Adaptor Proteins, Signal Transducing / metabolism
Antigens, CD / genetics*
Antigens, CD / metabolism*
Apoptosis
Carcinoma, Hepatocellular / genetics*
Carcinoma, Hepatocellular / metabolism*
Carcinoma, Hepatocellular / pathology
Cell Adhesion Molecules, Neuronal / antagonists & inhibitors
Cell Adhesion Molecules, Neuronal / genetics*
Cell Adhesion Molecules, Neuronal / metabolism*
Cell Line, Tumor
Cell Proliferation
Fetal Proteins / antagonists & inhibitors
Fetal Proteins / genetics*
Fetal Proteins / metabolism*
Gene Knockdown Techniques
Humans
Hyaluronan Receptors / genetics*
Hyaluronan Receptors / metabolism*
Liver Neoplasms / genetics*
Liver Neoplasms / metabolism*
Liver Neoplasms / pathology
NF-kappa B / metabolism*
Phosphoproteins / metabolism
RNA, Messenger / genetics
RNA, Messenger / metabolism
RNA, Neoplasm / genetics
RNA, Neoplasm / metabolism
Signal Transduction
Transcription Factors
Up-Regulation
YAP-Signaling Proteins

Substances

ALCAM protein, human
Adaptor Proteins, Signal Transducing
Antigens, CD
CD44 protein, human
Cell Adhesion Molecules, Neuronal
Fetal Proteins
Hyaluronan Receptors
NF-kappa B
Phosphoproteins
RNA, Messenger
RNA, Neoplasm
Transcription Factors
YAP-Signaling Proteins
YAP1 protein, human