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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
miR-335 inhibited cell proliferation of lung cancer cells by target Tra2β
Jian Liu1, Tingting Bian2, Jia Feng2
1Department of Chemotherapy, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Abstract:
Accumulating evidence has suggested that the dysregulation of miRNA is an important factor in the pathogenesis of lung cancer. Here, we demonstrate that miR-335 expression is reduced in non-small cell lung cancer (NSCLC) tumors relative to non-cancerous adjacent tissues, while the expression of Tra2β is increased. In addition, clinical data revealed that the increased Tra2β and decreased miR-335 expression observed in NSCLC cells was associated with poor patient survival rates. In vitro experimentation showed that the overexpression of miR-335 inhibited the growth, invasion and migration capabilities of A459 lung cancer cells, by targeting Tra2β. In contrast, inhibition of miR-335 or overexpression of the Tra2β target gene stimulated the growth, invasion and migratory capabilities of A459 lung cancer cells in vitro. Furthermore, overexpression of miR-335 or inhibition of Tra2β decreased the phosphorylation of Rb-S780 and Rb-AKT. Overall, these findings suggest that the downregulation of miR-335 in A459 lung cancer cells promoted cell proliferation through upregulation of Tra2β, mediated via activation of the AKT/mTOR signaling pathway, and suggest that miR-335 may have potential as a novel therapeutic target for NSCLC.
Insights
MicroRNA-335 (miR-335) downregulation in non-small cell lung cancer (NSCLC) promotes tumor growth by increasing Tra2β. Restoring miR-335 may offer a new therapeutic strategy for NSCLC.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- MicroRNA (miRNA) dysregulation is implicated in lung cancer pathogenesis.
- Specific miRNA roles in non-small cell lung cancer (NSCLC) require further elucidation.
Purpose of the Study:
- To investigate the role of miR-335 and its target Tra2β in NSCLC.
- To explore the potential of miR-335 as a therapeutic target for NSCLC.
Main Methods:
- Quantitative analysis of miR-335 and Tra2β expression in NSCLC tissues and cell lines.
- In vitro experiments involving miR-335 overexpression/inhibition and Tra2β manipulation in A549 cells.
- Assessment of cell proliferation, invasion, migration, and protein phosphorylation (Rb-S780, Rb-AKT).
Main Results:
- miR-335 was downregulated, and Tra2β was upregulated in NSCLC tumors, correlating with poor survival.
- miR-335 overexpression inhibited A549 cell growth, invasion, and migration by targeting Tra2β.
- Inhibition of miR-335 or Tra2β overexpression promoted A549 cell proliferation, invasion, and migration.
- miR-335/Tra2β modulation affected Rb-S780 and Rb-AKT phosphorylation, indicating AKT/mTOR pathway involvement.
Conclusions:
- Downregulation of miR-335 in NSCLC promotes proliferation via Tra2β upregulation and AKT/mTOR pathway activation.
- miR-335 represents a potential novel therapeutic target for NSCLC treatment.
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