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Mechanisms and therapeutic potential of YTHDF readers: Linking epitranscriptomics to cancer
Na Deng1,2, Qiang Sun3,4, Shuying Wang5
1Key Laboratory of Molecular Pathology and Epidemiology of Gastric Cancer in Liaoning Education Department, The First Hospital of China Medical University, Shenyang, 110001, China.
Abstract:
YT521-B homology domain-containing family paralogs (YTHDFs), as RNA epigenetic modification effector proteins, fully or partially participate in N6-methyladenosine (m6A), N1-methyladenosine (m1A), and 5-methylcytosine (m5C) modifications, which play critical roles in tumor biology and contribute to obtaining and maintaining cancer hallmarks relying on their characteristic protein structures. Accumulating evidence has underscored the involvement of YTHDFs in manipulating RNA stability, translation, and RNA metabolism, thereby influencing tumor initiation, progression, and anti-tumor treatment efficacy through independent RNA epigenetic modification pathways. This review aims to illustrate the essential regulatory mechanisms and pathological consequences of YTHDFs in tumorigenesis and therapeutic resistance. Additionally, we highlight the potential of targeting YTHDFs for cancer therapy, offering promising avenues for the elimination of tumor cells and the amelioration of tumor treatment efficacy.
Insights
YT521-B homology domain-containing family proteins (YTHDFs) are key players in RNA epigenetic modifications like m6A, influencing cancer development and treatment resistance. Targeting YTHDFs offers a promising strategy for effective cancer therapy.
Area of Science:
- Molecular Biology
- Cancer Biology
- Epigenetics
Background:
- YT521-B homology domain-containing family proteins (YTHDFs) act as effector proteins for RNA epigenetic modifications.
- YTHDFs are involved in N6-methyladenosine (m6A), N1-methyladenosine (m1A), and 5-methylcytosine (m5C) modifications.
- These modifications play critical roles in cancer biology and the maintenance of cancer hallmarks.
Purpose of the Study:
- To review the regulatory mechanisms and pathological consequences of YTHDFs in tumorigenesis.
- To explore the role of YTHDFs in therapeutic resistance.
- To highlight the potential of targeting YTHDFs for cancer therapy.
Main Methods:
- Literature review of accumulating evidence on YTHDFs.
- Analysis of YTHDFs' involvement in RNA stability, translation, and metabolism.
- Examination of YTHDFs' independent RNA epigenetic modification pathways.
Main Results:
- YTHDFs manipulate RNA stability, translation, and metabolism.
- YTHDFs influence tumor initiation, progression, and anti-tumor treatment efficacy.
- YTHDFs are implicated in therapeutic resistance.
Conclusions:
- YTHDFs are crucial in cancer development and progression.
- Targeting YTHDFs presents a promising strategy for cancer treatment.
- YTHDFs offer potential for eliminating tumor cells and improving treatment efficacy.
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