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1. OLA1 regulates epithelial-mesenchymal transition through the modulation of GSK-3β-Snail-E-cadherin signaling | |||
ZHANG Jiawei,BAI Li,CHENG Huarong,SHI Zhengzheng | |||
Clinical Medicine 15 December 2015 | |||
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Abstract:OLA1 is a member of the Obg family of P-loop NTPases with a putative GTPase-like molecular switch function. In this study the role of OLA1 in the regulation of epithelial-mesenchymal transition (EMT) was characterized in human lung cells and carcinomas. RNAi-mediated silencing of OLA1 rendered both A549 (lung adenocarcinoma-derived) and Beas-2B (noncancerous) cells resistant to transforming growth factor (TGF)-β1-induced transition to mesenchymal morphology accompanied, at molecular level, by reduced loss of epithelial marker E-cadherin and largely demolished Snail, the transcriptional repressor of E-cadherin. Because degradation of Snail is mediated by its phosphorylation by GSK-3, OLA1's effect on GSK-3 was further investigated. OLA1 was found to interact with GSK-3 and be involved in the phosphorylation (Ser9)-mediated GSK-3 deactivation. The protein-protein interaction required the presence of the OLA1 TGS domain, indicating TGS' novel function. These results suggest that OLA1 plays an important role in EMT, especially in lung epithelial cells and tumors, through regulating GSK-3β activity, Snail stability, and expression of E-cadherin. | |||
TO cite this article:ZHANG Jiawei,BAI Li,CHENG Huarong, et al. OLA1 regulates epithelial-mesenchymal transition through the modulation of GSK-3β-Snail-E-cadherin signaling[OL].[15 December 2015] http://en.paper.edu.cn/en_releasepaper/content/4669464 |
2. Epigenetic silencing of protocadherin 10 in colorectal cancer | |||
ZHANG Jiawei,ZHONG Xian,SHEN Hong,ZHENG Shu | |||
Clinical Medicine 15 December 2015 | |||
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Abstract:Colorectal cancer (CRC) is one of the leading malignant tumors in the world and known as a multi-step process resulting from the accumulation of both genetic and epigenetic alterations of the genome. Although the molecular mechanisms of its pathogenesis remain unclear, inactivation of tumor-suppressor genes (TSGs) through promoter methylation plays an important role in the development of CRC. Aberrant methylation is the most well-defined hallmark in CRC. Recently, epigenetic silencing of protocadherin 10 (PCDH10) was found, as a frequent and early event, in CRC. PCDH10 has been identified as an important tumor suppressor gene (TSG) with key roles of colorectal carcinogenesis, invasion and metastasis. The advantages of gene methylation as a target for detection and diagnosis in tumor tissues and body fluids have led to discovering non-invasive screening methods for CRC. This article aims mainly to review the epigenetic alteration of PCDH10 and the possibility of a non-invasive biomarker for CRC. | |||
TO cite this article:ZHANG Jiawei,ZHONG Xian,SHEN Hong, et al. Epigenetic silencing of protocadherin 10 in colorectal cancer[OL].[15 December 2015] http://en.paper.edu.cn/en_releasepaper/content/4669482 |
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