<P>Transmembrane protein 165 (TMEM165), a Golgi protein, functions in ion homeostasis and vesicular trafficking in the Golgi apparatus. While mutations in <I>TMEM165</I> are known to cause human ‘congenital disorders of glycosylati...
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https://www.riss.kr/link?id=A107456168
2018
-
SCI,SCIE,SCOPUS
학술저널
1297-1306(10쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
<P>Transmembrane protein 165 (TMEM165), a Golgi protein, functions in ion homeostasis and vesicular trafficking in the Golgi apparatus. While mutations in <I>TMEM165</I> are known to cause human ‘congenital disorders of glycosylati...
<P>Transmembrane protein 165 (TMEM165), a Golgi protein, functions in ion homeostasis and vesicular trafficking in the Golgi apparatus. While mutations in <I>TMEM165</I> are known to cause human ‘congenital disorders of glycosylation’, a recessive autosomal metabolic disease, the potential association of this protein with human cancer development has not been explored to date. In the present study, we revealed that <I>TMEM165</I> is overexpressed in HCC and its depletion weakens the invasive activity of cancer cells through suppression of matrix metalloproteinase-2 (MMP-2) expression. Levels of <I>TMEM165</I> mRNA and protein were clearly increased in HCC patient tissues and cell cultures. Quantitative real-time RT-PCR analysis of fresh HCC tissues (n=88) revealed association of <I>TMEM165</I> overexpression with more frequent macroscopic vascular invasion, microscopic serosal invasion and higher α-fetoprotein levels. Notably, depletion of <I>TMEM165</I> led to a marked decrease in the invasive activity of two different HCC cell types, Huh7 and SNU475, accompanied by downregulation of MMP-2. Our collective findings clearly indicated that TMEM165 contributed to the progression of HCC by promoting invasive activity, supporting its utility as a novel biomarker and therapeutic target for cancer.</P>