BACKGROUND: Receptor-interacting serine/threonine protein kinase-2 (RIPK2) has been reported to be an important regulator of tumor proliferation, differentiation and wound repair. We investigated the effects of RIPK2 knockdown in human hepatoma cells on epithelial-to-mesenchymal transition (EMT)-associated gene expression. MATERIALS AND METHODS: HepG2 cells stably expressing RIPK2-shRNA (HepG2-shRIPK2) were generated after puromycin selection. Total RNAs from HepG2-shRIPK2 and from HepG2-shcontrol cells were isolated and PCR-based arrays were performed to compare the 84 EMT-associated gene expressions. RESULTS: We observed that knockdown of RIPK2 down-regulated mRNA expression of jagged 1 (JAG1); plasminogen activator inhibitor-1 (PAI1); regulator of G-protein signalling 2, 24 kDa (RGS2); E-cadherin (CDH1); fibroblast growth factor binding protein 1 (FGFBP1); snail homolog 2 (SNAI2); protein tyrosine phosphatase type IVA, member 1 (PTP4A1); keratin 19 (KRT19); vimentin (VIM); and survival of motor neuron protein-interacting protein 1 (SIP1). CONCLUSION: We found that knockdown of RIPK2 down-regulated nuclear factor kappa B (NF-κB)-dependent PAI1 and VIM gene expressions. RIPK2 might play an important role in hepatic cell migration. These findings could shed new light on carcinogenesis and on liver regeneration.
BACKGROUND:Receptor-interacting serine/threonine protein kinase-2 (RIPK2) has been reported to be an important regulator of tumor proliferation, differentiation and wound repair. We investigated the effects of RIPK2 knockdown in humanhepatoma cells on epithelial-to-mesenchymal transition (EMT)-associated gene expression. MATERIALS AND METHODS: HepG2 cells stably expressing RIPK2-shRNA (HepG2-shRIPK2) were generated after puromycin selection. Total RNAs from HepG2-shRIPK2 and from HepG2-shcontrol cells were isolated and PCR-based arrays were performed to compare the 84 EMT-associated gene expressions. RESULTS: We observed that knockdown of RIPK2 down-regulated mRNA expression of jagged 1 (JAG1); plasminogen activator inhibitor-1 (PAI1); regulator of G-protein signalling 2, 24 kDa (RGS2); E-cadherin (CDH1); fibroblast growth factor binding protein 1 (FGFBP1); snail homolog 2 (SNAI2); protein tyrosine phosphatase type IVA, member 1 (PTP4A1); keratin 19 (KRT19); vimentin (VIM); and survival of motor neuron protein-interacting protein 1 (SIP1). CONCLUSION: We found that knockdown of RIPK2 down-regulated nuclear factor kappa B (NF-κB)-dependent PAI1 and VIM gene expressions. RIPK2 might play an important role in hepatic cell migration. These findings could shed new light on carcinogenesis and on liver regeneration.
Authors: Christopher M Browne; Baishan Jiang; Scott B Ficarro; Zainab M Doctor; Jared L Johnson; Joseph D Card; Sindhu Carmen Sivakumaren; William M Alexander; Tomer M Yaron; Charles J Murphy; Nicholas P Kwiatkowski; Tinghu Zhang; Lewis C Cantley; Nathanael S Gray; Jarrod A Marto Journal: J Am Chem Soc Date: 2018-12-20 Impact factor: 15.419
Authors: Nagore I Marín-Ramos; Thu Zan Thein; Hee-Yeon Cho; Stephen D Swenson; Weijun Wang; Axel H Schönthal; Thomas C Chen; Florence M Hofman Journal: Mol Cancer Ther Date: 2018-02-13 Impact factor: 6.261