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miR-148a increases the sensitivity to cisplatin by targeting Rab14 in renal cancer cells
Eun-Ae Kim1, Tae Ghab Kim1, Eon-Gi Sung1
1Department of Anatomy, College of Medicine, Yeungnam University, Nam-Gu, Daegu 705-717, Republic of Korea.
Abstract:
MicroRNA (miR) can exert various biological functions by targeting oncogenes or tumor suppressor genes in numerous human malignancies. Recent evidence has shown that miR-148a increases the drug sensitivity of various cancer cells. Herein, we show that ectopic expression of miR-148a induces apoptosis, reduces clonogenicity, and increases the sensitivity to TRAIL and cisplatin in renal cancer cells. The luciferase reporter assay showed that miR-148a negatively regulated ras-related protein 14 (Rab14) expression by binding to the miR-148a binding site in the 3' untranslated region (3'UTR) of Rab14. Rab14-specific siRNA-induced downregulation of Rab14 increases the sensitivity to cisplatin, while forced expression of Rab14 lacking 3'-UTR abrogated the pro-apoptotic function of miR-148a in renal cancer cells. These findings suggest that miR-148a acts as a tumor suppressor and holds great potential for renal cancer therapy by directly targeting Rab14.
Insights
MicroRNA-148a enhances renal cancer cell sensitivity to chemotherapy by targeting the Rab14 gene. This microRNA acts as a tumor suppressor, offering potential for novel renal cancer therapies.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- MicroRNAs (miRNAs) regulate gene expression and are implicated in various human cancers.
- miR-148a has emerged as a potential sensitizer to anti-cancer drugs in different malignancies.
- Understanding miRNA roles is crucial for developing targeted cancer therapies.
Purpose of the Study:
- To investigate the role of miR-148a in renal cancer.
- To determine if miR-148a affects the sensitivity of renal cancer cells to chemotherapy and apoptosis-inducing agents.
- To identify the direct molecular targets of miR-148a in renal cancer.
Main Methods:
- Ectopic expression of miR-148a in renal cancer cells.
- Assays for apoptosis, clonogenicity, and drug sensitivity (TRAIL, cisplatin).
- Luciferase reporter assays to confirm direct targeting of Rab14 by miR-148a.
- RNA interference (siRNA) to downregulate Rab14 and rescue experiments with Rab14 constructs.
Main Results:
- Ectopic miR-148a expression induced apoptosis and reduced clonogenicity in renal cancer cells.
- miR-148a significantly increased sensitivity to TRAIL and cisplatin.
- Luciferase assays confirmed miR-148a directly targets the 3'UTR of Rab14, negatively regulating its expression.
- Downregulation of Rab14 using siRNA enhanced cisplatin sensitivity, and Rab14 overexpression abrogated miR-148a's pro-apoptotic effects.
Conclusions:
- miR-148a functions as a tumor suppressor in renal cancer.
- miR-148a exerts its tumor-suppressive effects by directly targeting Rab14.
- miR-148a holds significant therapeutic potential for renal cancer treatment.
