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TERE1/UBIAD1的下调激活了Ras-MAPK信号通路并诱导细胞增殖。

Down-regulation of TERE1/UBIAD1 activated Ras-MAPK signalling and induced cell proliferation.

作者信息

Xia Yanzhi, Wei Xiong, Wu Shimin, Wang Bo, Wang Ximing, Hong Ling

机构信息

College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, Peoples Republic of China ; †Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Peoples Republic of China.

出版信息

Cell Biol Int Rep (2010). 2010;17(1):e00005. doi: 10.1042/CBR20100005. Epub 2010 Nov 8.

DOI:10.1042/CBR20100005
PMID:23119142
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3475436/
Abstract

TERE1/UBIAD1 is involved in SCCD (Schnyder crystalline corneal dystrophy) and multiple human cancers. So far, the molecular mechanism of TERE1/UBIAD1 in tumourigenesis is unclear. Here, the expression levels of hTERT and TERE1/UBIAD1 in pathologically proven Chinese TCC (transitional cell carcinoma) samples were measured. It was found that decreased TERE1/UBIAD1 expression is closely related to both an increased hTERT expression and activation of Ras-MAPK signalling. Chemically modified TERE1 siRNA oligos were used to knock down TERE1 expression in human L02 cells. Cells transfected with TERE1 siRNA oligos underwent significant cell proliferation. When the levels of hTERT expression and ERK phosphorylation were measured, it was found that both of them increased in the above transfected cells, suggesting the activation of Ras-MAPK signalling. Addition of the MEK inhibitor U0126 into the transfected L02 cells described above inhibited ERK phosphorylation and hTERT expression. Our result is the initial demonstration that down-regulation of TERE1 activates Ras-MAPK signalling and induces subsequent cell proliferation. TERE1 might be a new negative regulator of Ras-MAPK signalling, which plays a pivotal role in the cell proliferation of multiple human cancers.

摘要

TERE1/UBIAD1与施奈德结晶性角膜营养不良（SCCD）及多种人类癌症相关。迄今为止，TERE1/UBIAD1在肿瘤发生中的分子机制尚不清楚。在此，我们检测了经病理证实的中国移行细胞癌（TCC）样本中hTERT和TERE1/UBIAD1的表达水平。结果发现，TERE1/UBIAD1表达降低与hTERT表达增加及Ras-MAPK信号通路激活密切相关。使用化学修饰的TERE1 siRNA寡核苷酸来敲低人L02细胞中的TERE1表达。转染TERE1 siRNA寡核苷酸的细胞出现显著的细胞增殖。当检测hTERT表达水平和ERK磷酸化水平时，发现上述转染细胞中二者均增加，提示Ras-MAPK信号通路被激活。向上述转染的L02细胞中添加MEK抑制剂U0126可抑制ERK磷酸化和hTERT表达。我们的结果首次证明TERE1的下调激活Ras-MAPK信号通路并诱导随后的细胞增殖。TERE1可能是Ras-MAPK信号通路的一种新的负调节因子，在多种人类癌症的细胞增殖中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/6d6122413c10/cbr017e005f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/e84557c750d6/cbr017e005f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/5445a55b546f/cbr017e005f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/ae4129ab5ae7/cbr017e005f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/b0d943c5bc2d/cbr017e005f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/6d6122413c10/cbr017e005f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/e84557c750d6/cbr017e005f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/5445a55b546f/cbr017e005f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/ae4129ab5ae7/cbr017e005f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/b0d943c5bc2d/cbr017e005f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd48/3475436/6d6122413c10/cbr017e005f05.jpg

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