C-kit signaling promotes proliferation and invasion of colorectal mucinous adenocarcinoma in a murine model

摘要: // Jun Tan 1, 2 , Shu Yang 2, 3 Ping Shen Haimei Sun Jie Xiao Yaxi Wang Bo Wu Fengqing Ji Jihong Yan 1 Hong Xue Deshan Zhou Department of Histology and Embryology, School Basic Medical Sciences, Capital University, Beijing 100069, P. R. China Key Laboratory Cancer Invasion Metastasis Research, Institute Correspondence to: Zhou, e-mail: zhoudeshan2008@163.com Keywords: colorectal mucinous adenocarcinoma, C-kit, ETV4, murine model Received: March 24, 2015      Accepted: August 20, Published: September 02, 2015 ABSTRACT It was reported that the receptor tyrosine kinase (RTK) family often highly expressed in several carcinomas. In present study, we established a adenocardinoma (CRMAC) by treating C57 mice [both wild type (WT) loss-of-function c-kit mutant (Wads −/− )] with AOM+DSS for 37 weeks found c-kit, member RTK family, clearly enhanced tumor cell proliferation decreasing p53 increasing cyclin D1 through AKT pathway. Significantly, strongly promoted invasiveness which induced MMP7 expression epithelial-mesenchymal transition (EMT) via ERK vitro up- or down-regulating activation human cancer HCT-116 cells further consolidated these results. conclusion, our data suggested signaling obviously invasion CRMAC. Therefore, targeting its downstream molecules might provide potential strategies treatment patients suffering from CRMAC future.