ArticleCancer research and treatment2026
RMRP-Induced Chemoresistance in Relapsed and Refractory Acute Myeloid Leukemia via Mitochondrial Dysfunction.
Article in Cancer research and treatment, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: Relapsed and refractory acute myeloid leukemia (R/R AML) has a poor prognosis due to chemotherapy resistance. Mitochondrial dysfunction contributes to this resistance, but the role of the RNA component of mitochondrial RNA processing endoribonuclease (RMRP) in R/R AML remains unclear. Materials and Methods: Mass spectrometry identified molecules linked to chemoresistance in AML. The role of RMRP was examined by assessing its impact on mitochondrial transfer in the AML bone marrow microenvironment. Transmission electron microscopy and western blotting were used to study mitochondrial function and autophagy in RMRP-knockdown AML cells. Results: RMRP was overexpressed in R/R AML, and its silencing sensitized AML cells to chemotherapy drugs. RMRP knockdown reduced mitochondrial respiratory capacity, mitochondrial DNA copy numbers, and mitochondrial gene transcription. It also led to altered mitophagy markers and increased mitochondrial DNA methylation. Immunoprecipitation revealed RMRP-telomerase reverse transcriptase complex formation, suggesting a role in post-transcriptional regulation of mitochondrial function and reactive oxygen species production. Conclusion: High RMRP expression in R/R AML is linked to mitochondrial dysfunction and chemotherapy resistance, providing new insights into potential therapeutic strategies to overcome drug resistance in this disease.
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