miR-203a-3p-DNMT3B feedback loop facilitates non-small cell lung cancer progression.
Pingshan YangDongdong ZhangFengli ZhouWenyou ChenChuang HuDuqing XiaoSong-Wang CaiPublished in: Human cell (2022)
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.
Keyphrases
- cell proliferation
- small cell lung cancer
- dna methylation
- advanced non small cell lung cancer
- transcription factor
- poor prognosis
- cell cycle arrest
- brain metastases
- gene expression
- cell cycle
- induced apoptosis
- oxidative stress
- endoplasmic reticulum stress
- long non coding rna
- signaling pathway
- risk assessment
- tyrosine kinase
- circulating tumor cells