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Multiple Copies in T-Cell Malignancy 1 (MCT-1) Promotes the Stemness of Non-Small Cell Lung Cancer Cells via Activating Interleukin-6 (IL-6) Signaling through Suppressing MiR-34a Expression
被引:6
|作者:
Li, Yonghuai
[1
]
Wang, Baolin
[2
]
Gui, Shuyu
[1
]
Ji, Juanjuan
[1
]
机构:
[1] Anhui Med Univ, Affiliated Hosp 1, Dept Resp & Crit Care Med, Hefei, Anhui, Peoples R China
[2] Anhui Med Univ, Mol Biol Lab, Hefei, Anhui, Peoples R China
来源:
关键词:
Lung Neoplasms;
MicroRNAs;
Neoplastic Stem cells;
Receptors;
Interleukin-6;
METASTASIS;
D O I:
10.12659/MSM.919690
中图分类号:
R-3 [医学研究方法];
R3 [基础医学];
学科分类号:
1001 ;
摘要:
Background: Although the oncogenic roles of multiple copies in T-cell malignancy 1 (MCT-1) have been revealed in multiple cancers, its effects on non-small cell lung cancer (NSCLC) progression are still uncertain. This study aimed to reveal the effects of MCT-1 on the stem cell-like traits of NSCLC cells. Material/Methods: Western blot, real-time quantitative polymerase chain reaction (RT-qPCR), spheroid forming ability, and ALDH1 (aldehyde dehydrogenase 1) activity analysis were carried out to examine the effects of MCT-1/micrRNa-34 (miR-34a)/interleukin-6 (IL-6) on the stem cell-like characteristics of lung cancer cells. Results: MCT-1 knockdown reduced the spheroid forming ability, characterized as the decreased spheroid size and number. Additionally, MCT-1 knockdown decreased the expression of the NSCLC stemness markers and the activity of ALDH1. Moreover, MCT-1 knockdown decreased IL-6 secretion that promotes NSCLC cell stemness. Furthermore, MCT-1 knockdown increased the level of miR-34a, which attenuated the stemness of NSCLC cells through targeting IL-6R (IL-6 receptor) expression. Conclusions: These results suggest MCT-1/miR-34a/IL-6/IL-6R axis is responsible for MCT-1-mediated effects on NSCLC cell stemness.
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页码:10198 / 10204
页数:7
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