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miR-21-5p promotes lung adenocarcinoma progression partially through targeting SET/TAF-Iα
Jiacheng Zhong1, Xiaohu Ren1, Zhihong Chen1
1Institute of Toxicology, Shenzhen Center for Disease Control and Prevention, No 8 Longyuan Road, Nanshan District, Shenzhen 518055, Guangdong, China.
Objective:
Although SET(I2PP2A) and miRNAs are reported to play a pivotal role in lung cancer, the underlying mechanisms have remained obscure. To address this issue, we investigated how miRNAs and SET participate in the progression of lung cancer.
Methods:
miRNAs that target SET were predicted from multiple miRNA databases. Three human NSCLC cell lines and two normal lung cell lines were used to evaluate aberrant miRNA and SET expressions. A dual luciferase reporter assay system was employed to verify the interaction between miRNA and SET. Stable miRNA knockdown and SET overexpression in A549 cells were achieved through lentivirus transfection; the corresponding influences on lung cancer progression were also examined.
Results:
In this study, A549 was the sole cell line to lack SET/TAF-Iα expression, which was inversely correlated with the up-regulation of miR-21-5p. SET was subsequently revealed as the direct target site of miR-21-5p in A549 cells. The stable miR-21-5p knockdown and SET/TAF-Iα overexpression were shown to markedly enhance the expression of SET/TAF-Iα and to inhibit the migration, invasion, proliferation as well as the in vivo tumorigenicity of A549 cells.
Conclusion:
We suggest that SET/TAF-Iα might be a tumor suppressing factor regulated by miR-21-5p in lung adenocarcinoma. This might provide a target for lung adenocarcinoma therapy.
Insights
MicroRNA-21-5p (miR-21-5p) regulates SET/TAF-Iα, a tumor suppressor, in lung adenocarcinoma. This interaction inhibits cancer progression and may offer a therapeutic target for lung cancer.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- SET (also known as TAF-Iα) and microRNAs (miRNAs) are implicated in lung cancer pathogenesis.
- The precise molecular mechanisms involving SET and miRNAs in lung cancer progression remain largely unelucidated.
Purpose of the Study:
- To investigate the regulatory relationship between miRNAs and SET in lung cancer.
- To determine the functional role of this interaction in lung cancer progression.
Main Methods:
- Prediction of miRNA targets for SET using bioinformatics databases.
- Expression analysis of miRNAs and SET in non-small cell lung cancer (NSCLC) and normal lung cell lines.
- Validation of the miRNA-SET interaction using dual-luciferase reporter assays.
- Functional studies involving stable miR-21-5p knockdown and SET/TAF-Iα overexpression in A549 lung cancer cells.
Main Results:
- SET/TAF-Iα expression was inversely correlated with miR-21-5p up-regulation in A549 cells, identifying SET as a direct target of miR-21-5p.
- Overexpression of SET/TAF-Iα and knockdown of miR-21-5p significantly inhibited A549 cell migration, invasion, proliferation, and in vivo tumorigenicity.
- SET/TAF-Iα expression was enhanced by miR-21-5p knockdown.
Conclusions:
- SET/TAF-Iα functions as a tumor suppressor in lung adenocarcinoma.
- miR-21-5p negatively regulates SET/TAF-Iα, promoting lung cancer progression.
- Targeting the miR-21-5p/SET axis presents a potential therapeutic strategy for lung adenocarcinoma.
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