OSMR induces M2 polarization of glioblastoma associated macrophages through JAK/STAT3 signaling pathway.

ABSTRACT:

Introduction

Verify whether Onconstatin M receptor (OSMR) plays a regulatory role in the growth of glioblastoma (GBM) and explore its specific regulatory mechanism.

Methods

In vitro investigations were carried out using OSMR knockdown and treatment with JAK agonist Butyzamide (JAKa). Evaluate cell proliferation rate through CCK-8; Colony formation experiment to detect cell proliferation; Transwell experiment evaluates cell invasion; Cell scratch assay to detect cell migration; WB detects the expression levels of pathway related proteins JAK, p-JAK, STAT3, p-STAT3, and CCL-2; Flow cytometry analysis of apoptosis rate, cell cycle arrest rate, and proportion of M2 macrophages; RT-qPCR was implemented to identify the expression of M2 polarization factors CD206, CD163 and

SUBMITTER: Xiao C 

PROVIDER: S-EPMC11949811 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature