Blocking microRNA may slow bladder cancer growth

A study by researchers at the D’Or Institute for Research and Education in Rio de Janeiro, Brazil, suggests that blocking the microRNA known as miR-21 may significantly slow the growth and spread of bladder cancer cells, pointing toward a promising therapeutic pathway for one of the most recurrent and difficult-to-treat malignancies.

Lead author Paulo R. M. Dos Santos, Ph.D., and colleagues set out to determine whether inhibiting miR-21 could restore the function of a natural tumor-suppressing gene called RECK, which is responsible for regulating enzymes that break down tissue structures and enable cancer cells to invade surrounding healthy tissue.

The findings, published in Biochemical Genetics earlier this year, revealed when miR-21 is overexpressed, RECK is suppressed, which may help fuel tumor progression.

To test their hypothesis, the research team used a high-grade urothelial carcinoma cell line commonly employed in bladder cancer research. They introduced a specific inhibitor designed to block miR-21 activity, then measured changes in gene expression, protein levels, cell proliferation and cell migration.

The results showed that reducing miR-21 levels led to a marked increase in RECK expression and a corresponding decrease in MMP9, an enzyme associated with tumor invasion and aggressive cancer behavior. Functional assays further demonstrated that bladder cancer cells treated with the miR-21 inhibitor had significantly reduced ability to migrate and form new colonies, indicating slower tumor-growth potential.

According to Dos Santos, the findings highlight the potential of miR-21 as both a biomarker and a targeted therapy candidate. He noted that miR-21 overexpression has consistently been observed in bladder tumor samples compared with healthy tissue and that its suppression may open the door to new treatment frameworks focused on modifying the tumor environment at the genetic and molecular level.

Bladder cancer is among the most common cancers worldwide and is known for high recurrence rates and treatment challenges. Many patients undergo repeated surgical procedures to remove tumors, endure intensive monitoring through cystoscopy and imaging, and may require intravesical therapies or systemic chemotherapy. For aggressive or high-grade disease, treatment may involve removal of the bladder, with significant impact on quality of life.

Because current treatment strategies often focus on controlling recurrence rather than preventing progression, the potential to interrupt cancer-cell behavior at the molecular level has generated substantial interest in oncology.

If validated in further research, blocking miR-21 could complement or reduce reliance on invasive surgical approaches or aggressive systemic therapy.

Dos Santos and his colleagues caution that although the results are compelling, the research remains at an early stage. The work was conducted in laboratory models and has not yet been tested in animal studies or human trials. Before clinical use can be considered, researchers will need to determine optimal dosing and delivery methods for miR-21 inhibitors and assess whether the approach is safe and effective in living systems.

Still, they wrote, their the findings deepen the understanding of molecular drivers in bladder cancer and support the exploration of novel therapeutic strategies targeting microRNA activity.

Because miR-21 overexpression has been found in other cancer types, including lung, breast and colorectal cancers, the researchers believe the mechanism could have broader applications as well.

The study concludes that increasing RECK expression through miR-21 inhibition may represent a viable strategy for slowing bladder cancer progression and merits further investigation.

Looking ahead, the research team plans to explore the effect of miR-21 inhibition in more complex biological models and hopes that continued work will eventually support clinical trial development.