LASS2 impairs proliferation of glioma stem cells and migration and invasion of glioma cells mainly via inhibition of EMT and apoptosis promotion

LAG1 longevity assurance homolog 2 (LASS2), a highly conserved transmembrane protein, has been reported in several cancer types. However, the roles of LASS2 in glioma biology remain elusive. In the present study, we investigated the expression of LAAS2 in human glioma tissues and the effects of LASS...

Full description

Saved in:
Bibliographic Details
Published inJournal of Cancer Vol. 13; no. 7; pp. 2281 - 2292
Main Authors Zhao, Wei-Jiang, Fan, Yi-Pu, Ou, Guan-Yong, Qiao, Xin-Yu
Format Journal Article
LanguageEnglish
Published Australia Ivyspring International Publisher 01.01.2022
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:LAG1 longevity assurance homolog 2 (LASS2), a highly conserved transmembrane protein, has been reported in several cancer types. However, the roles of LASS2 in glioma biology remain elusive. In the present study, we investigated the expression of LAAS2 in human glioma tissues and the effects of LASS2 on glioma stem cell (GSC) proliferation. Roles of LASS2 in glioma cell migration and invasion were also researched both and . Our results demonstrated that the level of LASS2 is gradually reduced with the increase of glioma grade. The level of LASS2 is significantly lower in GSCs than in non GSCs, whereas overexpression reduced the sphere formation and promoted the differentiation of CD133 glioblastoma cells, as was indicated by reduced levels of CD133 and Nestin. In addition, overexpression significantly reduced colony formation, migration, and invasion of glioma cells by promoting tumor cell apoptosis and inhibiting epithelial-mesenchymal transition (EMT). Overexpression of inhibited U-87 MG cell-derived glioma xenograft growth in nude mice in a manner similar to . Our findings indicate that LASS2 can function as a suppressor of glioma growth, suggesting that modulation of expression may contribute to a novel strategy for the management of glioma via inhibition of GSCs.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
These authors contributed equally to this article.
Competing Interests: The authors have declared that no competing interest exists.
ISSN:1837-9664
1837-9664
DOI:10.7150/jca.71256