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Updated: Sep 5, 2025

A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues
Published on: December 5, 2016
RNA N6-methyladenosine modification in regulating cancer stem cells and tumor immune microenvironment and its
Subhadra Kumari1, Santosh Kumar1, Srinivasan Muthuswamy2
1Department of Life Science, National Institute of Technology, Rourkela, India.
Abstract:
Therapy resistance is a well-known phenomenon in cancer treatment. It can be intrinsic or acquired, accountable for frequent tumor relapse and death worldwide. The interplay between cancer cells and their neighboring environment can activate complex signaling mechanisms influencing epigenetic changes and maintain cancer cell survival leading to the malignant phenotype. Cancer stem cells (CSCs) are tumor-initiating cells (TICs) and constitute the primary source of drug resistance and tumor recurrence. Studies have shown that cancer cells exhibit dysregulated RNA N6-methyladenosine (m6A) "writers," "erasers," and "readers" levels after acquiring drug resistance. The present review provides novel insight into the role of m6A modifiers involved in CSC generation, cancer cell proliferation, and therapy resistance. m6A RNA modifications in the cross-talk between CSC and the tumor immune microenvironment (TIME) have also been highlighted. Further, we have discussed the therapeutic potential of targeting m6A machinery for cancer diagnosis and the development of new therapies for cancer treatment.
Insights
Cancer stem cells (CSCs) drive therapy resistance by altering RNA modifications. Targeting these RNA N6-methyladenosine (m6A) pathways offers new strategies for cancer treatment and diagnosis.
Area of Science:
- Oncology
- Epigenetics
- Molecular Biology
Background:
- Therapy resistance is a major challenge in cancer treatment, leading to relapse and mortality.
- Cancer stem cells (CSCs) are key drivers of drug resistance and tumor recurrence.
- Dysregulated RNA N6-methyladenosine (m6A) modifications are observed in drug-resistant cancer cells.
Purpose of the Study:
- To review the role of m6A modifiers in CSC generation, proliferation, and therapy resistance.
- To explore the interplay between m6A modifications, CSCs, and the tumor immune microenvironment (TIME).
- To discuss the therapeutic potential of targeting the m6A machinery in cancer.
Main Methods:
- Literature review focusing on m6A RNA modifications and cancer stem cells.
- Analysis of signaling pathways influenced by the tumor microenvironment.
- Examination of epigenetic changes related to drug resistance.
Main Results:
- m6A modifiers play a crucial role in CSC generation and maintenance.
- Aberrant m6A levels contribute to cancer cell survival and therapy resistance.
- m6A modifications influence the cross-talk between CSCs and the TIME.
Conclusions:
- Targeting m6A machinery presents a promising therapeutic strategy for overcoming cancer drug resistance.
- Understanding m6A regulation in CSCs can lead to novel diagnostic and therapeutic approaches.
- m6A modification is a critical factor in cancer progression and treatment outcomes.
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