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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MiR-30 suppresses lung cancer cell 95D epithelial mesenchymal transition and invasion through targeted regulating
1Department of Respiratory Medicine, The Second Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, China. yunhuazhongzxx@163.com.
Objective:
As an important factor regulating the epithelial mesenchymal transition (EMT) Snail is associated with lung cancer. Bioinformatics analysis showed that microRNA-30a (miR-30a) may target the 3'-UTR of Snail mRNA. It was exhibited that miR-30a down-regulation was related to tumor size, TNM stage, and poor prognosis of non-small cell lung cancer (NSCLC) patients, which suggests that miR-30a might participate in NSCLC attack. This study aims to explore the role of miR-30a and Snail in NSCLC invasion and metastasis.
Patients And Methods:
NSCLC tumor and para-carcinoma tissues were collected from 46 patients to evaluate the miR-30a and Snail expressions. The targeted relationship between miR-30a and Snail was verified by using dual-luciferase reporter assay. 95D cells were cultured in vitro and transfected with miR-30a mimic or small interfere RNA targeting Snail (si-Snail). The expression of miR-30a, Snail, EMT-related factors, malignant growth, invasion, and apoptosis, were compared.
Results:
Snail was significantly up-regulated, while miR-30a was significantly reduced in NSCLC tissue. MiR-30a suppressed Snail expression by targeting the 3'-URT of Snail mRNA. 95D cells exhibited significantly higher Snail, N-cadherin, and vimentin levels, while lower miR-30a, E-cadherin, and occludin expressions were compared with 95C cells. 95D cells presented stronger malignant growth and invasive ability, whereas lower background apoptosis than 95C. MiR-30a mimic and/or si-Snail transfection significantly enhanced E-cadherin and occludin expression, while significantly declined N-cadherin and vimentin levels, thus weakening malignant growth and invasion and increasing cell apoptosis.
Conclusions:
Snail up-regulated, while miR-30a declined in NSCLC tissue. MiR-30a may suppress Snail expression, restrain EMT, and inhibit lung cancer cell invasion.
Insights
MicroRNA-30a (miR-30a) is reduced in non-small cell lung cancer (NSCLC), where it suppresses Snail expression. Restoring miR-30a inhibits epithelial mesenchymal transition (EMT), reducing NSCLC invasion and metastasis.
Area of Science:
- Molecular Oncology
- Cancer Biology
- Gene Regulation
Background:
- Snail is a key regulator of epithelial mesenchymal transition (EMT) and is implicated in lung cancer progression.
- MicroRNA-30a (miR-30a) has been observed to be downregulated in non-small cell lung cancer (NSCLC) and is predicted to target Snail mRNA.
- Downregulation of miR-30a correlates with advanced tumor stage and poor prognosis in NSCLC patients.
Purpose of the Study:
- To investigate the role of miR-30a and Snail in the invasion and metastasis of non-small cell lung cancer (NSCLC).
- To elucidate the regulatory relationship between miR-30a and Snail in NSCLC.
Main Methods:
- Expression levels of miR-30a and Snail were analyzed in NSCLC tissues and adjacent normal tissues from 46 patients.
- The direct targeting of Snail mRNA by miR-30a was confirmed using a dual-luciferase reporter assay.
- In vitro experiments involved transfecting 95D NSCLC cells with miR-30a mimic or small interfering RNA against Snail (si-Snail) to assess effects on EMT markers, cell proliferation, invasion, and apoptosis.
Main Results:
- Snail expression was significantly upregulated, while miR-30a expression was significantly downregulated in NSCLC tissues compared to controls.
- MiR-30a directly suppressed Snail expression by binding to its 3'-untranslated region (3'-UTR).
- Restoration of miR-30a or suppression of Snail in NSCLC cells reversed EMT markers, reduced malignant growth and invasion, and increased apoptosis.
Conclusions:
- Snail upregulation and miR-30a downregulation are characteristic of NSCLC tissue.
- MiR-30a acts as a tumor suppressor by inhibiting Snail expression, thereby restraining EMT and reducing lung cancer cell invasion.
- Targeting the miR-30a/Snail axis presents a potential therapeutic strategy for NSCLC.
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