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MiR-103a-3p aggravates renal cell carcinoma by targeting TMEM33
Jingyu Zhang1, Qingbo Lu2, Haigang Pang3
1Department of Urology, The Fourth People's Hospital of Shenyang Shenyang 110031, Liaoning Province, China.
Objective:
We investigated the mechanism of miR-103a-3p-mediated renal cell carcinoma (RCC) progression.
Methods:
The miR-103a-3p expressions were measured in clinical samples and in two RCC cell lines. MiR-103a-3p was inhibited or over-expressed in the 786-O and UO31 cell lines, respectively.
Results:
We found that miR-103a-3p is closely related to the development of RCC cells. A bioinformatics analysis and a dual-luciferase reporter gene assay revealed that there is a direct interaction between TMEM33 and miR-103a-3p. Moreover, a rescue assay further confirmed that TMEM33 overexpression can attenuate miR-103a-3p-induced RCC cell development.
Conclusion:
miR-103a-3p exerts a carcinogenic function in RCC by regulating TMEM33, a finding that may provide new insights into the development of prognostic markers and therapeutic targets for RCC.
Insights
MicroRNA-103a-3p promotes renal cell carcinoma (RCC) progression by targeting TMEM33. This finding offers potential new biomarkers and therapeutic strategies for RCC patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Renal cell carcinoma (RCC) is a significant global health concern.
- Understanding the molecular mechanisms driving RCC progression is crucial for developing effective treatments.
Purpose of the Study:
- To elucidate the role of microRNA-103a-3p (miR-103a-3p) in renal cell carcinoma (RCC) progression.
- To identify the downstream targets and regulatory pathways involved in miR-103a-3p-mediated RCC development.
Main Methods:
- Quantitative analysis of miR-103a-3p expression in clinical RCC samples and cell lines.
- In vitro manipulation of miR-103a-3p levels (inhibition/overexpression) in RCC cell lines (786-O and UO31).
- Bioinformatics analysis, dual-luciferase reporter assays, and rescue experiments to investigate the interaction between miR-103a-3p and TMEM33.
Main Results:
- miR-103a-3p expression levels were found to be closely associated with RCC development.
- A direct interaction between TMEM33 and miR-103a-3p was confirmed through bioinformatics and experimental assays.
- Overexpression of TMEM33 effectively counteracted the pro-cancer effects of miR-103a-3p in RCC cells.
Conclusions:
- miR-103a-3p functions as an oncomiR in RCC, promoting cancer progression by regulating TMEM33.
- The miR-103a-3p/TMEM33 axis represents a potential target for novel prognostic markers and therapeutic interventions in RCC.
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