title: Cluster of differentiation 166 (CD166) regulates cluster of differentiation (CD44) via NF-κB in liver cancer cell line Bel-7402.
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.
authors.affiliation: Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, PR China. Electronic address: malifang0606118@126.com.
authors.forename: Lifang
authors.initials: L
authors.lastname: Ma
authors.affiliation: Department of Central Laboratory, Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, PR China. Electronic address: panqiuhui123@126.com.
authors.forename: Qiuhui
authors.initials: Q
authors.lastname: Pan
authors.affiliation: Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, PR China. Electronic address: sunfenyong@126.com.
authors.forename: Fenyong
authors.initials: F
authors.lastname: Sun
authors.affiliation: Shanghai Municipal Hospital of Traditional Chinese Medicine Affiliated to Shanghai TCM University, Shanghai 200071, PR China. Electronic address: yueyongchun88@163.com.
authors.forename: Yongchun
authors.initials: Y
authors.lastname: Yu
authors.affiliation: Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, PR China. Electronic address: karajan2@163.com.
authors.forename: Jiayi
authors.initials: J
authors.lastname: Wang
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D015703:Antigens, CD / Q000235:genetics* / Q000378:metabolism*; D017209:Apoptosis; D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D015816:Cell Adhesion Molecules, Neuronal / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism*; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D005326:Fetal Proteins / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism*; D055785:Gene Knockdown Techniques; D006801:Humans; D018960:Hyaluronan Receptors / Q000235:genetics* / Q000378:metabolism*; D008113:Liver Neoplasms / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism*; D010750:Phosphoproteins / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012334:RNA, Neoplasm / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D014157:Transcription Factors; D015854:Up-Regulation; D000091102:YAP-Signaling Proteins; D020410:Activated-Leukocyte Cell Adhesion Molecule
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D015703:Antigens, CD; D015816:Cell Adhesion Molecules, Neuronal; D005326:Fetal Proteins; D018960:Hyaluronan Receptors; D016328:NF-kappa B; D010750:Phosphoproteins; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D014157:Transcription Factors; D000091102:YAP-Signaling Proteins; C105613:ALCAM protein, human; D020410:Activated-Leukocyte Cell Adhesion Molecule; C497483:CD44 protein, human; C088374:YAP1 protein, human
keywords: COP1; Protein degradation; Signaling pathway; Transcription factor; UBC3