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Updated: Dec 21, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MicroRNA-365 inhibits the progression of lung adenocarcinoma through targeting ETS1 and inactivating AKT/mTOR pathway
1Department of Respiratory Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, P.R. China. lj198132@163.com.
Objective:
MicroRNAs (miRNAs) act as important regulators in human cancers by regulating the gene expression. The dysregulation of miR-365 has been investigated in many cancers. However, the function of miR-365 remains unknown in lung adenocarcinoma. Therefore, the regulatory mechanism of miR-365 was explored in lung adenocarcinoma.
Patients And Methods:
The expression of miR-365 was detected in cell lines and 67 lung adenocarcinoma tissues using qRT-PCR. The Kaplan-Meier analysis was used to determine the association between miR-365 expressions and the survival rate in patients with lung adenocarcinoma. Transwell assay was then performed to investigate the effect of miR-365 on invasion and migration of lung adenocarcinoma cells.
Results:
Downregulation of miR-365 and upregulation of ETS1 were identified in lung adenocarcinoma. Furthermore, miR-365 reversely regulated ETS1 expression in lung adenocarcinoma. Functionally, the overexpression of miR-365 inhibited proliferation, migration, and invasion of lung adenocarcinoma cells. However, the upregulation of ETS1 lessened the inhibitory effect of miR-365 in lung adenocarcinoma. In addition, miR-365 inhibited EMT and inactivated AKT/mTOR pathway in lung adenocarcinoma.
Conclusions:
MiR-365 inhibits the progression of lung adenocarcinoma by targeting ETS1 and inactivating the AKT/mTOR pathway.
Insights
MicroRNA-365 (miR-365) inhibits lung adenocarcinoma progression by targeting ETS1 and the AKT/mTOR pathway. This finding offers new insights into lung cancer regulation and potential therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- MicroRNAs (miRNAs) are key regulators of gene expression implicated in human cancers.
- Dysregulation of miR-365 is observed in various cancers, but its role in lung adenocarcinoma is unclear.
- Understanding miR-365's mechanism is crucial for developing targeted lung cancer therapies.
Purpose of the Study:
- To investigate the regulatory mechanism of miR-365 in lung adenocarcinoma.
- To determine the functional role of miR-365 in lung adenocarcinoma cell behavior.
- To elucidate the molecular pathways targeted by miR-365.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to assess miR-365 and ETS1 expression in cell lines and patient tissues.
- Kaplan-Meier analysis to correlate miR-365 expression with patient survival.
- Transwell assays to evaluate the impact of miR-365 on cell migration and invasion.
Main Results:
- miR-365 was downregulated, while ETS1 was upregulated in lung adenocarcinoma.
- Overexpression of miR-365 suppressed proliferation, migration, and invasion of lung adenocarcinoma cells.
- miR-365 inhibited epithelial-mesenchymal transition (EMT) and inactivated the AKT/mTOR pathway, with ETS1 upregulation counteracting these effects.
Conclusions:
- miR-365 acts as a tumor suppressor in lung adenocarcinoma.
- The inhibitory effect of miR-365 on lung adenocarcinoma progression is mediated through targeting ETS1 and inactivating the AKT/mTOR pathway.
- miR-365 represents a potential therapeutic target for lung adenocarcinoma.
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