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Research Paper|Volume 13, Issue 7|pp 9780—9800

Lung cancer-associated mesenchymal stem cells promote tumor metastasis and tumorigenesis by induction of epithelial–mesenchymal transition and stem-like reprogram

Cihui Yan1, Jingjing Chang1, Xinmiao Song2, Ying Qi1, Zhenyu Ji1, Ting Liu1, Wenwen Yu1, Feng Wei1, Lili Yang1, Xiubao Ren1
  • 1Department of Immunology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Ti-Yuan-Bei, He Xi 300060, Tianjin, China
  • 2Department of Electromyogram, 3rd Affiliated Hospital of Hebei Medical University, Shijiazhuang 050051, Hebei, China
Received: May 7, 2020Accepted: February 9, 2021Published: March 19, 2021

Copyright: © 2021 Yan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Mesenchymal stem cells (MSCs) have attracted more attention in antitumor therapy by using MSCs as vehicles or targeting modulators of MSCs. But their role and mechanisms in tumor progression are less known. In the present study, we successfully isolated pairs of MSCs from lung cancer (LC-MSCs) and adjacent tumor-free tissues. Based on the coculture system in vitro and animal studies in vivo, we originally found that LC-MSCs significantly promoted tumor metastasis and tumorigenesis both in vitro and in vivo. Partial epithelial–mesenchymal transition (EMT) was induced in lung cancer cells by LC-MSCs by the evidence of remarkable increase in snail and slug expression but not in other EMT-associated genes. The expression of stem related genes also escalated significantly. And spheroids perfectly formed when tumor cells were co-incubated with LC-MSCs. These results revealed a close link of partial EMT and acquisition of stem-like traits in lung cancer cells which was induced by LC-MSCs and greatly promoted metastasis and tumorigenesis in lung cancer. Our findings provided a new insight into LC-MSCs in tumor progression and helped to identify LC-MSCs as a potential vehicle or target for lung cancer therapy.