N6-methyladenosine (m6A) is the most abundant internal chemical modification of eukaryotic mRNA and plays diverse roles in gene regulation. The m6A modification plays a significant role in numerous cancer types, including kidney, stomach, lung, bladder tumors, and melanoma, through varied mechanisms. As direct m6A readers, the YT521-B homology domain family proteins (YTHDFs) play a key role in tumor transcription, translation, protein synthesis, tumor stemness, epithelial-mesenchymal transition (EMT), immune escape, and chemotherapy resistance. An in-depth understanding of the molecular mechanism of YTHDFs is expected to provide new strategies for tumor treatment. In this review, we provide a systematic description of YTHDF protein structure and its function in tumor progression.
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http://dx.doi.org/10.3389/fgene.2022.934223 | DOI Listing |
J Biochem Mol Toxicol
February 2025
Department of Neurosurgery, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Objective: Gliomas are the predominant form of malignant brain tumors. We investigated the mechanism of hypoxia-inducible factor-1α (HIF-1α) affecting glioma metabolic reprogramming, proliferation and invasion.
Methods: Human glioma cell U87 was cultured under hypoxia and treated with small interfering (si)HIF-1α, si-B cell lymphoma-2/adenovirus E1B 19-kDa interacting protein 3 (siBNIP3), si-YT521-B homology domain 2 (siYTHDF2), 3-methyladenine and 2-deoxyglucose, with exogenous sodium lactate-treated normally-cultured cells as a lactate-positive control.
Plants (Basel)
December 2024
State Key Laboratory of Tree Genetics and Breeding, Nanjing Forestry University, Nanjing 210037, China.
-methyladenosine (mA) is a widespread post-transcriptional modification of RNA in eukaryotes. The conserved YTH-domain-containing RNA binding protein has been widely reported to serve as a typical mA reader in various species. However, no studies have reported the mA readers in ().
View Article and Find Full Text PDFMol Biomed
December 2024
Department of Hematology, Shanxi Bethune Hospital, Third Hospital of Shanxi Medical University, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Taiyuan, 030032, China.
Millions of people worldwide die of acute myeloid leukaemia (AML) each year. Although N6-methyladenosine (mA) modification has been reported to regulate the pathogenicity of AML, the mechanisms by which mA induces dysfunctional hematopoietic differentiation in elderly AML patients remain elusive. This study elucidates the mechanisms of the mA landscape and the specific roles of mA regulators in hematopoietic cells of elderly AML patients.
View Article and Find Full Text PDFEMBO J
December 2024
University of Copenhagen, Copenhagen Plant Science Center, Department of Biology, Copenhagen N, Denmark.
N6-methyladenosine (mA) exerts many of its regulatory effects on eukaryotic mRNAs by recruiting cytoplasmic YT521-B homology-domain family (YTHDF) proteins. Here, we show that in Arabidopsis thaliana, the interaction between mA and the major YTHDF protein ECT2 also involves the mRNA-binding ALBA protein family. ALBA and YTHDF proteins physically associate via a deeply conserved short linear motif in the intrinsically disordered region of YTHDF proteins and their mRNA target sets overlap, with ALBA4 binding sites being juxtaposed to mA sites.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Dermatology, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China; General Practice Department, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. Electronic address:
YT521-B homology domain family 2 (YTHDF2), a pivotal m6A-binding protein, is now understood to significantly influence a diverse array of biological functions, including cell migration, proliferation, differentiation, and inflammatory responses. Additionally, YTHDF2 participates in mRNA decay and pre-rRNA processing. This study explored the specific role of YTHDF2 in the pathogenesis of psoriasis and its underlying mechanisms.
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