BACKGROUND: MicroRNA-145 (miR-145) has been reported to be a tumor-suppressing agent in several studies. It can repress pluripotency and control human embryonic stem cell differentiation by regulating the core pluripotency factor OCT4. However, it is not known whether miR-145 can play a role in inducing tumor cell differentiation and repressing growth of tumors. METHODS: Ishikawa cells, the established human endometrial cancer cells, were treated with miR-145 mimics, inhibitor, or small interfering RNA OCT4. miR-145 levels were assayed using TaqMan microRNA assays, and the messenger RNA levels of OCT4 and the differentiation marker glycodelin were measured using real-time polymerase chain reaction. The protein levels of OCT4 and glycodelin were characterized via flow cytometry, western blotting, and immunohistochemistry. In vivo activity was measured in a xenograft mouse model. RESULTS: Up-regulating miR-145 reduced the expression of OCT4 and induced the differentiation of Ishikawa cells to closely resemble normal endometrial epithelium both in vitro and in vivo. miR-145 successfully inhibited tumor growth. We also found that in patients with endometrial carcinoma, miR-145 and OCT4 were expressed in tissues, and there was a relationship between miR-145, OCT4, and the degree of tumor cell differentiation. CONCLUSIONS: Our results strongly suggested that miR-145 is a tumor cell differentiation-inducing agent in endometrial carcinoma, and that miR-145 or OCT4 may be useful markers for grading endometrial carcinoma. Cancer 2011
BACKGROUND:MicroRNA-145 (miR-145) has been reported to be a tumor-suppressing agent in several studies. It can repress pluripotency and control human embryonic stem cell differentiation by regulating the core pluripotency factor OCT4. However, it is not known whether miR-145 can play a role in inducing tumor cell differentiation and repressing growth of tumors. METHODS: Ishikawa cells, the established humanendometrial cancer cells, were treated with miR-145 mimics, inhibitor, or small interfering RNA OCT4. miR-145 levels were assayed using TaqMan microRNA assays, and the messenger RNA levels of OCT4 and the differentiation marker glycodelin were measured using real-time polymerase chain reaction. The protein levels of OCT4 and glycodelin were characterized via flow cytometry, western blotting, and immunohistochemistry. In vivo activity was measured in a xenograft mouse model. RESULTS: Up-regulating miR-145 reduced the expression of OCT4 and induced the differentiation of Ishikawa cells to closely resemble normal endometrial epithelium both in vitro and in vivo. miR-145 successfully inhibited tumor growth. We also found that in patients with endometrial carcinoma, miR-145 and OCT4 were expressed in tissues, and there was a relationship between miR-145, OCT4, and the degree of tumor cell differentiation. CONCLUSIONS: Our results strongly suggested that miR-145 is a tumor cell differentiation-inducing agent in endometrial carcinoma, and that miR-145 or OCT4 may be useful markers for grading endometrial carcinoma. Cancer 2011
Authors: Tai-Chung Huang; Santosh Renuse; Sneha Pinto; Praveen Kumar; Yi Yang; Raghothama Chaerkady; Brian Godsey; Joshua T Mendell; Marc K Halushka; Curt I Civin; Luigi Marchionni; Akhilesh Pandey Journal: Mol Biosyst Date: 2014-10-30
Authors: Sathivel Chinnathambi; Susan Wiechert; Ann Tomanek-Chalkley; Michael C Winter; Jackie R Bickenbach Journal: J Dermatol Date: 2012-04-09 Impact factor: 4.005
Authors: M Cioce; F Ganci; V Canu; A Sacconi; F Mori; C Canino; E Korita; B Casini; G Alessandrini; A Cambria; M A Carosi; R Blandino; V Panebianco; F Facciolo; P Visca; S Volinia; P Muti; S Strano; C M Croce; H I Pass; G Blandino Journal: Oncogene Date: 2013-11-18 Impact factor: 9.867