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

Med Sci Monit. 2019 Dec 31:25:10198-10204. doi: 10.12659/MSM.919690.

Abstract

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 AND 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.

MeSH terms

  • A549 Cells
  • Carcinoma, Non-Small-Cell Lung / genetics
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Cell Cycle Proteins / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Gene Knockdown Techniques
  • Humans
  • Interleukin-6 / metabolism*
  • Lung Neoplasms / genetics
  • Lung Neoplasms / pathology*
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Neoplastic Stem Cells / metabolism
  • Neoplastic Stem Cells / pathology*
  • Oncogene Proteins / metabolism*
  • Receptors, Interleukin-6 / metabolism
  • Signal Transduction*

Substances

  • Cell Cycle Proteins
  • IL6R protein, human
  • Interleukin-6
  • MCTS1 protein, human
  • MIRN34 microRNA, human
  • MicroRNAs
  • Oncogene Proteins
  • Receptors, Interleukin-6