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10.1002/jcp.26267

http://scihub22266oqcxt.onion/10.1002/jcp.26267
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C6055661!6055661!29150940
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suck abstract from ncbi


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pmid29150940      J+Cell+Physiol 2018 ; 233 (10): 6565-77
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  • Tumor?suppressive roles of ?Np63??miR?205 axis in epithelial?mesenchymal transition of oral squamous cell carcinoma via targeting ZEB1 and ZEB2 #MMPMID29150940
  • Hashiguchi Y; Kawano S; Goto Y; Yasuda K; Kaneko N; Sakamoto T; Matsubara R; Jinno T; Maruse Y; Tanaka H; Morioka M; Hattori T; Tanaka S; Kiyoshima T; Nakamura S
  • J Cell Physiol 2018[Oct]; 233 (10): 6565-77 PMID29150940show ga
  • We previously revealed that epithelial?to?mesenchymal transition (EMT) was mediated by ?Np63?, a splicing variant of ?Np63, in oral squamous cell carcinoma (OSCC). Recent studies have highlighted the involvement of microRNA (miRNA) in EMT of cancer cells, though the mechanism remains unclear. To identify miRNAs responsible for ?Np63??mediated EMT, miRNA microarray analyses were performed by ?Np63??overexpression in OSCC cells; SQUU?B, which lacks ?Np63 expression and displays EMT phenotypes. miRNAs microarray analyses revealed miR?205 was the most up?regulated following ?Np63??overexpression. In OSCC cells, miR?205 expression was positively associated with ?Np63 and negatively with zinc?finger E?box binding homeobox (ZEB) 1 and ZEB2, potential targets of miR?205. miR?205 overexpression by miR?205 mimic transfection into SQUU?B cells led to decreasing ZEB1, ZEB2, and mesenchymal markers, increasing epithelial markers, and reducing cell motilities, suggesting inhibition of EMT phenotype. Interestingly, the results opposite to this phenomenon were obtained by transfection of miR?205 inhibitor into OSCC cells, which express ?Np63 and miR?205. Furthermore, target protector analyses revealed direct regulation by miR?205 of ZEB1 and ZEB2 expression. These results showed tumor?suppressive roles of ?Np63? and miR?205 by inhibiting EMT thorough modulating ZEB1 and ZEB2 expression in OSCC.
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