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Updated: May 22, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Inhibition of autophagy and tumor growth in colon cancer by miR-502
1Department of Pathology, Translational Research Laboratory, Stony Brook University, Stony Brook, NY 11794-8691, USA.
Abstract:
Autophagy is a catabolic process that allows cellular macromolecules to be broken down and recycled as metabolic precursors. The influence of non-coding microRNAs in autophagy has not been explored in colon cancer. In this study, we discover a novel mechanism of autophagy regulated by hsa-miR-502-5p (miR-502) by suppression of Rab1B, a critical mediator of autophagy. A number of other miR-502 suppressed mRNA targets (for example, dihydroorotate dehydrogenase) are also identified by microarray analysis. Ectopic expression of miR-502 inhibited autophagy, colon cancer cell growth and cell-cycle progression of colon cancer cells in vitro. miR-502 also inhibited in-vivo colon cancer growth in a mouse tumor xenografts model. In addition, the expression of miR-502 was regulated by p53 via a negative feedback regulatory mechanism. The expression of miR-502 was downregulated in colon cancer patient specimens compared with the paired normal control samples. These results suggest that miR-502 may function as a potential tumor suppressor and therefore be a novel candidate for developing miR-502-based therapeutic strategies.
Insights
MicroRNA-502 (miR-502) suppresses autophagy and colon cancer growth by targeting Rab1B. This microRNA is downregulated in colon cancer patients, suggesting it acts as a tumor suppressor.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- Autophagy is a cellular process for macromolecule breakdown and recycling.
- The role of non-coding microRNAs in colon cancer-associated autophagy remains largely unexplored.
- Rab1B is identified as a key mediator in autophagy pathways.
Purpose of the Study:
- To investigate the novel mechanism of autophagy regulation by hsa-miR-502-5p (miR-502) in colon cancer.
- To identify miR-502-suppressed mRNA targets and their role in colon cancer.
- To evaluate the therapeutic potential of miR-502 in colon cancer models.
Main Methods:
- Microarray analysis to identify miR-502-suppressed mRNA targets.
- In vitro studies to assess the effects of ectopic miR-502 expression on colon cancer cells.
- In vivo mouse tumor xenograft models to evaluate miR-502's impact on tumor growth.
- Analysis of p53-mediated regulation of miR-502 expression.
Main Results:
- Ectopic miR-502 expression inhibited autophagy, colon cancer cell proliferation, and cell-cycle progression in vitro.
- miR-502 suppressed tumor growth in a mouse xenograft model.
- Microarray analysis identified Rab1B and dihydroorotate dehydrogenase as miR-502 targets.
- p53 was found to regulate miR-502 expression via negative feedback.
- miR-502 expression was significantly downregulated in colon cancer patient samples.
Conclusions:
- miR-502 acts as a novel regulator of autophagy by suppressing Rab1B.
- miR-502 demonstrates tumor-suppressive properties in colon cancer, inhibiting cell growth and progression.
- Downregulation of miR-502 in patient samples suggests its potential role as a biomarker.
- miR-502 represents a promising candidate for developing novel therapeutic strategies against colon cancer.
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