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miR-133a & miR-135a Shows Promise in Pediatric AML Therapy

May, 05, 2024 | AML (Acute Myeloid Leukemia), Leukemia

KEY TAKEAWAYS

  • The study aimed to investigate the role of miR-133a and miR-135a in pediatric AML pathogenesis and their potential as therapeutic targets to improve patient outcomes.
  • Researchers noticed that miR-133a and miR-135a hold promise as prognostic markers and therapeutic targets in pediatric AML.

Acute myeloid leukemia (AML) is a type of blood cancer characterized by the rapid proliferation of immature myeloid cells. Despite advancements in treatment, the prognosis for pediatric AML remains unfavorable, highlighting the urgent need for deeper insights into its underlying mechanisms and the development of novel therapeutic strategies to improve patient outcomes.

Yu-Cai Cheng and the team aimed to assess the regulatory effects of miR-133a and miR-135a on CDX2 translation and their impact on all-trans retinoic acid (ATRA)-mediated differentiation in pediatric AML.

They performed an inclusive analysis using quantitative reverse-transcription PCR to quantify the expression levels of microRNA (miR)-133a and miR-135a in 68 samples obtained from 59 pediatric patients diagnosed with AML. Additionally, they employed dual-luciferase reporter transfection assays, Cell Counting Kit-8 assays, and western blot analysis to investigate the functional roles of miR-133a and miR-135a in pediatric AML.

All-trans-retinoic acid (ATRA) promoted the expression of miR-133a and miR-135a in AML cells. It inhibited caudal-type homeobox 2 (CDX2) expression, subsequently suppressing the proliferation of AML cells. Moreover, miR-133a and miR-135a exhibited high expression levels in patients who achieved complete remission and those with better survival.

The study concluded that miR-133a and miR-135a may exert an anti-oncogenic role in pediatric AML via the ATRA-miRNA133a/135a-CDX2 pathway. These findings suggest their potential as favorable prognostic indicators and novel therapeutic targets for improving outcomes in pediatric AML patients.

The funding was sponsored by the Medical Science and Technology Research Foundation of Guangdong Province, China, the Shenzhen Fundamental Research Program.

Source: https://pubmed.ncbi.nlm.nih.gov/38693824/

Cheng YC, Fan Z, Liang C, et al. (2024). “miR-133a and miR-135a Regulate All-Trans Retinoic Acid-Mediated Differentiation in Pediatric Acute Myeloid Leukemia by Inhibiting CDX2 Translation and Serve as Prognostic Biomarkers.” Technol Cancer Res Treat. 2024

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