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

IF 4.3 3区生物学

Human Cell Pub Date : 2022-07-01 Epub Date: 2022-06-07 DOI:10.1007/s13577-022-00728-y

Pingshan Yang, Dongdong Zhang, Fengli Zhou, Wenyou Chen, Chuang Hu, Duqing Xiao, Songwang Cai

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引用次数: 2

Abstract

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.

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miR-203a-3p-DNMT3B反馈回路促进非小细胞肺癌癌症进展

据报道，microRNA-203a-3p（miR-203a-3p）可调节多种癌细胞类型的细胞增殖、迁移和侵袭。然而，人们对其在肺癌进展中的作用知之甚少。本研究发现，miR-203a-3p 在非小细胞肺癌（NSCLC）细胞系和组织中下调。在体外，miR-203a-3p 的过表达可抑制 NSCLC 细胞的增殖、迁移和侵袭，并促进细胞凋亡。恢复 miR-203a-3p 在 A549 和 NCI-H520 细胞中的表达可增强它们的化疗敏感性。进一步的实验表明，DNA甲基转移酶3B（DNMT3B）是miR-203a-3p的直接靶标。此外，本研究结果还揭示了启动子高甲基化是导致 miR-203a-3p 在 NSCLC 中低表达的潜在机制。值得注意的是，在 NSCLC 中观察到了 miR-203a-3p 和 DNMT3B 之间的反馈调节。此外，miR-203a-3p 的过表达会降低肿瘤在体内的生长。总之，本研究发现了一个促进 NSCLC 进展的 miR-203a-3p-DNMT3B 反馈环路。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Human Cell 生物-细胞生物学

CiteScore

6.60

自引率

2.30%

发文量

176

期刊介绍： Human Cell is the official English-language journal of the Japan Human Cell Society. The journal serves as a forum for international research on all aspects of the human cell, encompassing not only cell biology but also pathology, cytology, and oncology, including clinical oncology. Embryonic stem cells derived from animals, regenerative medicine using animal cells, and experimental animal models with implications for human diseases are covered as well. Submissions in any of the following categories will be considered: Research Articles, Cell Lines, Rapid Communications, Reviews, and Letters to the Editor. A brief clinical case report focusing on cellular responses to pathological insults in human studies may also be submitted as a Letter to the Editor in a concise and short format. Not only basic scientists but also gynecologists, oncologists, and other clinical scientists are welcome to submit work expressing new ideas or research using human cells.