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Colorectal Cancer Puzzle: m6A Modification and Its Intricate Relationship With Drug Resistance
Mengxiang Yang1, Zhihui Dai1,2, Yuejun Han1
1Department of Colorectal Surgery, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, 321000 Jinhua, Zhejiang, China.
N6-methyladenosine (m6A) RNA modification is crucial in colorectal cancer (CRC) development and treatment resistance. Understanding m6A dysregulation offers new therapeutic strategies for CRC patients.
Area of Science:
- Molecular Biology
- Oncology
- Epigenetics
Background:
- Colorectal cancer (CRC) incidence and mortality are rising globally.
- N6-methyladenosine (m6A) is the most abundant internal RNA modification, regulating gene expression post-transcriptionally.
- Dysregulated m6A is increasingly linked to CRC progression and treatment failure.
Purpose of the Study:
- To review m6A biogenesis and regulatory mechanisms.
- To discuss the role of m6A dysregulation in CRC pathogenesis, metastasis, and therapeutic resistance.
- To highlight m6A's impact on resistance to chemotherapy, targeted therapy, and immunotherapy.
Main Methods:
- Literature review of m6A modification in eukaryotes.
- Analysis of m6A-related factors in CRC.
- Examination of m6A's role in mediating treatment resistance.
Main Results:
- m6A modification is dynamically regulated by writers, erasers, and readers.
- Aberrant m6A patterns are associated with CRC development and metastasis.
- m6A plays a significant role in mediating resistance to various CRC therapies.
Conclusions:
- m6A dysregulation is a key factor in CRC pathogenesis and treatment resistance.
- Targeting m6A pathways presents a promising avenue for novel CRC therapies.
- Further research into m6A is essential for developing effective CRC treatment strategies.
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