Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 496, Issue 4, Pages 1169-1175Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2018.01.164
Keywords
microRNA-138; Cancer stem cells; Epithelial mesenchymal transition; Primary lung cancer cells
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Funding
- National Key Technology RD program [2015BAI12B12]
- National Natural Science Foundation of China [81602449]
- Henan Medical Science and Technique Foundation [201701030]
- Henan Provincial Scientific and technological project [162300410095]
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The existence of cancer stem cells within the tumor could lead to cancer therapy resistance. TGF beta 1 is considered as one of the most powerful players in the generation of CSCs through induction of epithelial-mesenchymal transition in different types of cancer including lung cancer, however, the detailed mechanisms by which TGF beta 1 contribute to EMT induction and CSC maintenance remains unclear. Here, we showed primary lung cancer cells treated by TGF beta 1 exhibit mesenchymal features, including morphology and expression of mesenchymal marker in a time-dependent manner. We also observed long-term TGF beta 1 exposure leads to an enrichment of a sub-population of CD44(+) CD90(+) cells which represent CSCs in lung cancer cells. Moreover, the differential expression microRNAs between CSCs and non-CSCs were identified using next-generation sequencing to screen key miRNAs which might contribute to TGF beta 1-induced EMT and CSCs generation. Among those differentially expressed miRNAs, the expression of microRNA-138 was time-dependently down-regulated by TGF beta 1 treatment. We further demonstrated primary lung cancer cells, in which we knockdown the expression of miR-138, exhibit mesenchymal phenotypes and stem cell properties. Taken together, these findings indicate TGF beta 1-induced down-regulation of microRNA-138 contributes to EMT in primary lung cancer cells, and suggest that miR-138 might serve as a potential therapeutic target. (C) 2018 Elsevier Inc. All rights reserved.
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