Abstract The present study investigated the inhibitory effect of human umbilical cord mesenchymal stem cells (hucMSCs) on the growth of lung cancer in mice and its relationship with the TLR4/NF-κB signalling pathway. A mouse model of Lewis lung cancer was constructed by inoculating mice with Lewis lung cancer cell suspension under the axilla. Twenty mice were randomly and evenly divided into experimental group and control group. The experimental group received a caudal vein injection of 1 × 106 hucMSCs each week for two consecutive weeks, and the control group, an equal amount of saline at the same time. Two weeks after treatment with hucMSCs, the mice were sacrificed and the tumour volume and tumour weight were recorded. Enzyme-linked immunosorbent assay was used to determine the IL-1, IL-6 and TNF-α contents in lung cancer tissues; real-time polymerase chain reaction, to measure the level of mRNA; and Western blotting, to determine the protein expression. The results showed that injection of hucMSCs inhibited the growth of Lewis lung cancer tissues, reduced Lewis lung cancer tissue weight, enhanced thymus index, and suppressed inflammatory responses. hucMSCs inhibited the expression of inflammatory factors IL-1, IL-6 and TNF-α by activating TLR4/NF-κB signalling pathway, and facilitated the expression of Bax. Moreover, huMSCs induced the expression of apoptogenic factor Bax by activating TLR4/NF-κB signalling pathway, and inhibited the expression of antiapoptotic factor bcl-2. The present study demonstrates that hucMSCs reduce inflammatory responses by mediating TLR4/NF-κB signalling pathway, promote apoptosis of tumour cells, and inhibit tumour proliferation in mice with Lewis lung cancer.

中文翻译：

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人脐带间充质干细胞通过 TLR4/NF-κB 信号通路抑制肺癌

摘要 本研究探讨人脐带间充质干细胞（hucMSCs）对小鼠肺癌生长的抑制作用及其与TLR4/NF-κB信号通路的关系。小鼠腋窝下接种Lewis肺癌细胞悬液，构建Lewis肺癌小鼠模型。20只小鼠随机均匀分为实验组和对照组。实验组连续两周每周接受1×106个hucMSCs尾静脉注射，对照组同时接受等量生理盐水。用hucMSCs治疗两周后，处死小鼠并记录肿瘤体积和肿瘤重量。采用酶联免疫吸附法测定肺癌组织中IL-1、IL-6、TNF-α的含量；实时聚合酶链反应，测量mRNA水平；和蛋白质印迹，以确定蛋白质表达。结果表明，注射hucMSCs可抑制Lewis肺癌组织的生长，降低Lewis肺癌组织重量，增强胸腺指数，抑制炎症反应。HucMSCs通过激活TLR4/NF-κB信号通路抑制炎症因子IL-1、IL-6和TNF-α的表达，促进Bax的表达。此外，huMSCs通过激活TLR4/NF-κB信号通路诱导凋亡因子Bax的表达，并抑制抗凋亡因子bcl-2的表达。本研究表明hucMSCs通过介导TLR4/NF-κB信号通路减轻炎症反应，促进肿瘤细胞凋亡，