Data from Oncostatin M Modulates the Mesenchymal–Epithelial Transition of Lung Adenocarcinoma Cells by a Mesenchymal Stem Cell-Mediated Paracrine Effect
Oncostatin M
DOI:
10.1158/0008-5472.c.6504120
Publication Date:
2024-03-12T22:59:30Z
AUTHORS (8)
ABSTRACT
<div>Abstract<p>Mesenchymal stem cells (MSC) are strongly associated with tumor progression and have been used as novel cell-based agents to deliver anticancer drugs tumors. However, controversies about the direct involvement of MSCs in suggest that mediate a cancer type-dependent manner. In this report, we analyzed functional interactions between human lung adenocarcinoma (LAC) determine therapeutic potential cancer. We showed effectively inhibited migration, invasion, cell-cycle several LAC cell lines. also enhanced mesenchymal–epithelial transition (MET) pathway, evidenced by reduction epithelial–mesenchymal transition-related markers cocultured or MSC-conditioned medium (MSC-CM). By cytokine array analysis, determined Oncostatin M (OSM), differentiation-promoting cytokine, was elevated MSC-CM derived from primary MSC cultures. Furthermore, OSM treatment had same effects on LAC, whereas neutralizing antibodies reversed them. Notably, short hairpin RNAs against STAT1, an important downstream target OSM, hindered OSM-dependent induction MET. <i>In vivo</i> xenograft studies indicated formation metastasis cells, hampered its inhibitory effects. conclusion, study is paracrine mediator MSC-dependent inhibition tumorigenicity activation MET cells. These may serve basis for development new interventions targeting <i>Cancer Res; 72(22); 6051–64. ©2012 AACR</i>.</p></div>
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