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HGS促进肿瘤生长，而HGS的卷曲螺旋结构域及其寡肽则抑制肿瘤生长。

HGS Promotes Tumor Growth, Whereas the Coiled-Coil Domain and Its Oligopeptide of HGS Suppress It.

作者信息

Ogura Kiyoshi, Kawashima Ikuo, Kasahara Kohji

机构信息

Biomembrane Group, Tokyo Metropolitan Institute of Medical Science, 6-1-2, Kamikitazawa, Setagaya-Ku, Tokyo 113-8613, Japan.

出版信息

Int J Mol Sci. 2025 Jan 17;26(2):772. doi: 10.3390/ijms26020772.

DOI:10.3390/ijms26020772
PMID:39859488
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11766344/
Abstract

We previously isolated a cDNA clone for galactosylceramide expression factor 1, which is the rat homologue of hepatocyte-growth-factor-regulated tyrosine kinase substrate (HGS) and induces galactosylceramide expression and morphological changes in COS-7 cells, and reported that overexpression of HGS induced morphological changes in canine kidney epithelial MDCK cells. HGS is a component of the endosomal sorting complexes required for transport machinery that mediates endosomal multivesicle body formation. In this study, the overexpression of HGS induced epithelial-mesenchymal transition and caused transformation in MDCK cells, whereas the overexpression of a coiled-coil domain of HGS inhibited induction of epithelial-mesenchymal transition by HGF stimulation. The overexpression of HGS in mouse melanoma B16 cells and human colorectal cancer COLO205 cells promoted cancer characteristic anchorage-independent cell growth ability and tumor growth, whereas the overexpression of the coiled-coil domain of HGS in these cells suppressed them. The oligopeptide OP12-462 constituting the coiled-coil domain suppressed the anchorage-independent cell growth ability and tumor growth of COLO205 cells. The coiled-coil domain of HGS and OP12-462 are novel tumor growth inhibitors that do not directly destroy cancer cells but rather inhibit only the anchorage-independent cell growth ability of cancer cells.

摘要

我们先前分离出了一个半乳糖神经酰胺表达因子1的cDNA克隆，它是肝细胞生长因子调节的酪氨酸激酶底物（HGS）的大鼠同源物，可诱导COS-7细胞中的半乳糖神经酰胺表达和形态变化，并报道HGS的过表达可诱导犬肾上皮MDCK细胞发生形态变化。HGS是介导内体多囊泡体形成的转运机制所需的内体分选复合物的一个组成部分。在本研究中，HGS的过表达诱导了MDCK细胞的上皮-间质转化并导致其发生转化，而HGS卷曲螺旋结构域的过表达则抑制了HGF刺激诱导的上皮-间质转化。HGS在小鼠黑色素瘤B16细胞和人结肠直肠癌COLO205细胞中的过表达促进了具有癌症特征的非贴壁依赖性细胞生长能力和肿瘤生长，而HGS卷曲螺旋结构域在这些细胞中的过表达则抑制了它们。构成卷曲螺旋结构域的寡肽OP12-462抑制了COLO205细胞的非贴壁依赖性细胞生长能力和肿瘤生长。HGS的卷曲螺旋结构域和OP12-462是新型的肿瘤生长抑制剂，它们不会直接破坏癌细胞，而是仅抑制癌细胞的非贴壁依赖性细胞生长能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/abc93e71002d/ijms-26-00772-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/8187ee0d7d9f/ijms-26-00772-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/d68ae16996dd/ijms-26-00772-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/ee31e5d236d6/ijms-26-00772-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/b940383a0aa9/ijms-26-00772-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/abc93e71002d/ijms-26-00772-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/8187ee0d7d9f/ijms-26-00772-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/d68ae16996dd/ijms-26-00772-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/ee31e5d236d6/ijms-26-00772-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/b940383a0aa9/ijms-26-00772-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/11766344/abc93e71002d/ijms-26-00772-g005.jpg

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