Lpha and C/EBPbeta are expected for Sebocyte differentiation and stratified squamous differentiation in adult mouse skin. PloS One 2010, five, e9837. [CrossRef] [PubMed] Sugahara, K.; Sadohara, T.; Sugita, M.; Iyama, K.; Takiguchi, M. Differential expression of CCAAT enhancer binding protein loved ones in rat alveolar epithelial cell proliferation and in acute lung injury. Cell Tissue Res. 1999, 297, 261?70. [CrossRef] [PubMed] Gombart, A.F.; Hofmann, W.K.; Kawano, S.; Takeuchi, S.; Krug, U.; Kwok, S.H.; Larsen, R.J.; Asou, H.; Miller, C.W.; Hoelzer, D.; et al. Mutations in the gene encoding the transcription element CCAAT/enhancer binding protein alpha in myelodysplastic syndromes and acute myeloid leukemias. Blood 2002, 99, 1332?340. [CrossRef] [PubMed] Halmos, B.; Huettner, C.S.; Kocher, O.; Ferenczi, K.; Karp, D.D.; Tenen, D.G. Down-regulation and antiproliferative PA-Nic custom synthesis function of C/EBPalpha in lung cancer. Cancer Res. 2002, 62, 528?34. [PubMed] Tada, Y.; Brena, R.M.; Hackanson, B.; Morrison, C.; Otterson, G.A.; Plass, C. Epigenetic modulation of tumor suppressor CCAAT/enhancer binding protein alpha activity in lung cancer. J. Natl. Cancer Inst. 2006, 98, 396?06. [CrossRef] [PubMed] ?2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is definitely an open access article distributed beneath the terms and situations in the Inventive Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
cellsArticleHigh Glucose Concentrations Negatively Regulate the IGF1R/Src/ERK Axis through the MicroRNA-9 in Colorectal CancerYa-Chun Chen 1, , Ming-Che Ou 2, , Chia-Wei Fang 3 , Tsung-Hsien Lee 1,4, Shu-Ling Tzeng 1, 1 two 3andInstitute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan; [email protected] Division of Hematology and Oncology, Tungs’ Taichung MetroHarbor Hospital, Taichung 435, Taiwan; [email protected] Division of Colon and Rectal Surgery, Division of Surgery, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Healthcare Foundation, Taichung 427, Taiwan; [email protected] Division of Obstetrics and Gynecology, Chung Shan Medical University Hospital, Taichung 402, Taiwan Correspondence: [email protected] (T.-H.L.); [email protected] (S.-L.T.); Tel.: +886-9-2082-3519 (T.-H.L.); +886-2-473-0022 (ext. 11607) (S.-L.T.) These authors contributed equally to this function.Received: 14 February 2019; Accepted: six April 2019; Published: 8 AprilAbstract: Research have revealed that people with hyperglycemia have a higher danger of colorectal cancer (CRC). Hyperglycemia might be accountable for supplying power to CRC cells. Having said that, the prospective molecular mechanism for this association remains unclear. Moreover, microRNA-9 (miR-9) features a tumor-suppressive function in CRC. Aberrant decreased expression of miR-9 is involved within the improvement and progression of malignancy triggered by a high glucose (HG) concentration. In this study, we applied an HG concentration to activate miR-9 downregulation in CRC cells. Our results indicated that miR-9 decreased the insulin-like growth factor-1 receptor (IGF1R)/Src signaling pathway and downstream cyclin B1 and N-cadherin but upregulated ODM-204 supplier E-cadherin. The HG concentration not just promoted cell proliferation, elevated the G1 population, and modulated epithelial-to-mesenchymal transition (EMT) protein expression and morphology but additionally promoted the cell migration and invasion capability of SW480 (low metastatic prospective) and SW620 (high metastatic prospective) cells. Moreover, low glucos.
