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The Inhibitory Effect of Lung Cancer Microenvironment on Self Senescence of BM-MSCs and Its Mechanism
Gao Zhuoyue1, He Jianxin1, Liu Yongqi1,2*, Lu Zhiwei1, Wu Zhiwei1, Luo Yali1, Zhang Liying1, Su Yun1, Xue Na1
1Provincial-Level Key Laboratory for Molecular Medicine of Major Diseases and the Prevention and Treatment with Traditional Chinese Medicine Research in Gansu Colleges and Universities, Gansu University of Chinese Medicine, Lanzhou 730000, China; 2Key Laboratory of Dunhuang Medicine and Transformation at Provincial and Ministerial Level, Lanzhou 730000, China
Abstract: This work was aimed at exploring the inhibition and regulating mechanism of lung cancer microenvironment on self senescence of bone marrow-derived mesenchymal stem cells (BM-MSCs). It was set up Transwell system in which BM-MSCs were co-cultured with A549 in an indirect way， to study the influence of lung cancer microenvironment on self senescence of BM-MSCs by cell morphology， cell proliferation assay and cell senescence dyeing experiment. Meanwhile， it was also studied the regulating mechanism of lung cancer microenvironment on BM-MSCs senescence by detecting telomerase mRNA level with qPCR and searching relating signaling pathways with Western blot technology， respectively. Our results of 7-days co-cultured indicated that， morphology of co-cultured bone marrow-derived mesenchymal stem cells (Co-MSCs) greatly turned to spindle-like shape from fibroblast- like shape. Meanwhile， the whirlpool-like spreading were replaced by colony-like spreading of Co-MSCs. Proliferation of Co-MSCs was increased as cells passaging. Meanwhile， senescence character in Co-MSCs was decreased compared with that in BM-MSCs as cells passaging. Further study showed that telomerase mRNA level in Co-MSCs was in lower， compared with that in BM-MSCs. It was significant difference statistically (P<0.01). The result of Western blot analysis showed that， as cells were passaged， the STAT3 proein and its phosphorylation levels in BM-MSCs were always lower than that in Co-MSCs， and Co-MSCs shown that higher gradually. It was significant difference statistically (P<0.05). Our results suggested that lung cancer microenvironment could induce BMMSCs differentiate towards immortal cells to help BM-MSCs escape from senescence. The underlying mechanism could be involved in the activation of STAT3 in Co-MSCs.
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