Non-Coding RNAs Are Implicit in Chronic Myeloid Leukemia Therapy Resistance

Area of Science:

• Hematology
• Molecular Biology
• Oncology

Background:

• Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm driven by the BCR-ABL1 fusion gene.
• Tyrosine kinase inhibitors (TKIs) have significantly improved CML patient outcomes, but therapy resistance remains a challenge.
• Non-coding RNAs (ncRNAs) are increasingly recognized for their role in cancer development and treatment resistance.

Purpose of the Study:

• To explore the role of aberrantly expressed ncRNAs in CML therapy resistance.
• To discuss the mechanisms by which ncRNAs influence TKI resistance in CML.
• To highlight the potential of targeting ncRNAs for novel CML therapies.

Main Methods:

• Review of current literature on ncRNAs in CML.
• Analysis of dysregulation patterns of microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs) in CML.
• Discussion of ncRNA-mediated mechanisms of TKI resistance.

Main Results:

• ncRNAs, including miRNAs, circRNAs, and lncRNAs, are frequently dysregulated in CML.
• Aberrantly expressed ncRNAs contribute to both BCR-ABL1 dependent and independent TKI resistance.
• Tumor-suppressing ncRNAs are often silenced, while oncogenic ncRNAs are overexpressed in CML.

Conclusions:

• ncRNAs play a significant role in the development and progression of TKI resistance in CML.
• Targeting specific ncRNAs may offer a promising strategy to overcome CML therapy resistance.
• Further research into ncRNA function and regulation is essential for advancing CML treatment.