RÉSUMÉ
Connexin (Cx), a multigene-encoded transmembrane protein family, forms either gap junctions ( GJ) or hemichannels (HC) to mediate intercellular communication in plasma mem¬brane between adjacent cells or interacts with proteins by its car- boxyl terminal in the cytoplasm to participate in the process of tumor cell proliferation, apoptosis, necrosis, invasion, metasta¬sis, drug resistance and stem cell characteristics.However, mi- slocalization of Cx in cytoplasm or nucleus often occurs in many tumors, and involved in the occurrence and development of tumors.Subcellular localization of Cx is affected by post-transla- tional modifications, including phosphorylation, ubiquitination, and acetylation.In this paper the classification and function of Cx, the relationship between subcellular localization of Cx and tumorigenesis and the regulation of post-translational modifica¬tion on Cx are reviewed in order to provide new ideas for the study of Cx as a potential target for cancer therapy.
RÉSUMÉ
Aim To observe whether paeonol can in-hibit fibronectin (FN) and intercellular cell adhension molecule-1 (ICAM-1) expressions in high glucose (HG)-induced glomerular mesangial cells(GMCs) via up-regulating CKIP-1 and activating the Nrf2 signaling pathway. Methods The effects of paeonol on the ex-pressions of CKIP-1,Nrf2,FN and ICAM-1 were eval-uated in GMCs treated with HG. Small interfering RNA was used to deplete CKIP-1 protein expression, and Western bolt was used to detect the expressions of Nrf2, HO-1 and SOD1. DHE fluorescent probe tech-nique was used to determine intracellular superoxide level. Results The protein levels of CKIP-1 and Nrf2 were elevated by paeonol in HG-treated GMCs. In the meanwhile,the expressions of Nrf2 downstream antiox-idant enzymes, i.e. HO-1 and SOD1, were also up-regulated by paeonol, which was accompanied by re-ductions of superoxide and H2O2levels. Importantly, paeonol reversed the excessive accumulation of FN and ICAM-1 in HG-induced GMCs. si-CKIP-1 decreased the up-regulation of Nrf2,HO-1 and SOD1 expressions during paeonol treatment, which was accompanied by increased superoxide and H2O2levels. Furthermore, si-CKIP-1 reversed the down-regulated levels of FN and ICAM-1 induced by paeonol. Conclusion Pae-onol inhibits the expressions of FN and ICAM-1 in HG-treated GMCs possibly by up-regulating CKIP-1 and activating the Nrf2 signaling pathway.