作者: Parthasarathy Chandrakesan , Nathaniel Weygant , Randal May , Dongfeng Qu , Harisha R. Chinthalapally
关键词: Stem cell 、 Epithelial–mesenchymal transition 、 Biology 、 Cancer research 、 Intestinal epithelium 、 Carcinogenesis 、 Colorectal cancer 、 Intestinal mucosa 、 Cancer 、 Adenocarcinoma
摘要: // Parthasarathy Chandrakesan 1 , 2 Nathaniel Weygant Randal May 4 Dongfeng Qu Harisha R. Chinthalapally Sripathi M. Sureban Naushad Ali Stan A. Lightfoot 3 Shahid Umar 5 Courtney W. Houchen Department of Medicine, University Oklahoma Health Sciences center, City, OK 73104, USA OU Cancer Institute, Pathology, Center, Veterans Affairs Medical Molecular and Integrative Physiology, Kansas KS, Correspondence to Houchen, M.D. e-mail: Courtney-houchen@ouhsc.edu Key words: Dclk1; self-renewal; pluripotency; EMT; miRNAs; tumorigenesis Received: August 18, 2014 Accepted: 21, Published: September 02, 2014 ABSTRACT Doublecortin-like kinase (Dclk1) is overexpressed in many cancers including colorectal cancer (CRC) andit specifically marks intestinal tumor stem cells. However, the role Dclk1 Apc mutant conditions still poorly understood. We demonstrate that expression Dclk1+ cells are significantly increased epithelium elderly Min /+ mice compared young wild type mice. Intestinal epithelial pluripotency, self-renewing ability, EMT. Furthermore, miRNAs dysregulated, onco-miRNAs with decreased suppressor miRNAs. In support these findings, knockdown attenuates adenomas adenocarcinoma by decreasing EMT indicating overexpression facilitates tumorigenesis. Knocking down weakens Dclk1-dependent processes for This study demonstrates critically involved facilitating enhancing pluripotency factors tumors it also provides a potential therapeutic target treatment cancer.