miR-203a-3p-DNMT3B feedback loop facilitates non-small cell lung cancer progression

It has been reported that microRNA-203a-3p (miR-203a-3p) modulates cell proliferation, migration and invasion in a variety of cancer cell types. However, little is known about its role in lung cancer progression. The present study found that miR-203a-3p was downregulated in non-small cell lung cance...

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Published in:Human cell : official journal of Human Cell Research Society 2022-07, Vol.35 (4), p.1219-1233
Main Authors: Yang, Pingshan, Zhang, Dongdong, Zhou, Fengli, Chen, Wenyou, Hu, Chuang, Xiao, Duqing, Cai, Songwang
Format: Article
Language:English
Subjects:
Apoptosis
Biomedical and Life Sciences
Carcinoma, Non-Small-Cell Lung - genetics
Carcinoma, Non-Small-Cell Lung - pathology
Cell Biology
Cell Line, Tumor
Cell migration
Cell Movement - genetics
Cell proliferation
Cell Proliferation - genetics
DNA (Cytosine-5-)-Methyltransferases - genetics
DNA methyltransferase
DNA Methyltransferase 3B
Feedback
Gene Expression Regulation, Neoplastic
Gynecology
Humans
Life Sciences
Lung cancer
Lung Neoplasms - genetics
Lung Neoplasms - pathology
MicroRNAs - genetics
miRNA
Non-small cell lung carcinoma
Oncology
Reproductive Medicine
Research Article
Small cell lung carcinoma
Stem Cells
Surgery
Tumor cell lines
Tumors
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Summary:It has been reported that microRNA-203a-3p (miR-203a-3p) modulates cell proliferation, migration and invasion in a variety of cancer cell types. However, little is known about its role in lung cancer progression. The present study found that miR-203a-3p was downregulated in non-small cell lung cancer (NSCLC) cell lines and tissues. Overexpression of miR-203a-3p inhibits NSCLC cell proliferation, migration and invasion, and promotes cellular apoptosis in vitro. Restoration of miR-203a-3p expression in A549 and NCI-H520 cells enhances their chemosensitivity. Further experiments showed that DNA methyltransferase 3B (DNMT3B) was a direct target of miR-203a-3p. In addition, the present results revealed that promoter hypermethylation was the potential mechanism responsible for low miR-203a-3p expression in NSCLC. Notably, feedback regulation between miR-203a-3p and DNMT3B was observed in NSCLC. Moreover, Overexpression of miR-203a-3p reduces tumor growth in vivo. In summary, the present study has identified an miR-203a-3p-DNMT3B feedback loop that facilitates NSCLC progression.
ISSN:1749-0774
0914-7470
1749-0774
DOI:10.1007/s13577-022-00728-y