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

Abstract

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 in vitro and in vivo. 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 LASS2 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, LASS2 overexpression significantly reduced colony formation, migration, and invasion of glioma cells by promoting tumor cell apoptosis and inhibiting epithelial-mesenchymal transition (EMT). Overexpression of LASS2 inhibited U-87 MG cell-derived glioma xenograft growth in nude mice in a manner similar to in vitro. Our findings indicate that LASS2 can function as a suppressor of glioma growth, suggesting that modulation of LASS2 expression may contribute to a novel strategy for the management of glioma via inhibition of GSCs.

Integrative analysis of bulk RNA‐seq and scRNA‐seq data indicates the prognostic and immunologic values of SERPINH1 in glioma

“…Current research and the latest WHO classification standards indicate the value of identifying specific biomarkers for prognosis prediction and treatment. 4,21 The aberrant expression of SERPINH1, a gene encoding for a serine protease inhibitor, is associated with tumor progression due to its role in collagen biosynthesis. 22 Prior research indicated that SER-PINH1 is upregulated in various cancerous growths.…”

“…However, the etiopathogenesis of glioma remains unclear. Current research and the latest WHO classification standards indicate the value of identifying specific biomarkers for prognosis prediction and treatment 4,21 …”

Glioblastoma microenvironment and its reprogramming by oncolytic virotherapy

“…Thus, rQNestin 34.5v2, also a second-generation oHSV, deletes one copy under the control of the nestin promoter simultaneously as the double deletion of the γ134.5 (Nakashima et al, 2015). Nestin is a hallmark molecule in gliomas and is not expressed in other neuronal cells (Zhao et al, 2022). Another mutant that overcomes the insufficient replication capacity of G207 is G47∆, a thirdgeneration oHSV.…”