YTHDF1 (YTH N6-Methyladenosine RNA Binding Protein 1)

After controlling for potential confounders, including WHO grade, tumor volume, BDNF levels, and radiotherapy dose, carriers of the G allele (A/G + G/G genotypes) at rs6090311 demonstrated a significantly lower risk of developing post-radiotherapy cognitive dysfunction (OR = 0.319, 95% CI: 0.111-0.916). YTHDF1 overexpression is associated with post-radiotherapy cognitive dysfunction in glioma patients, and the rs6090311 G allele may act as a protective genetic marker for this complication.

Silencing METTL3 inhibits the malignant biological progression of PCa by mediating GDF15 via a YTHDF1-dependent m6A mechanism. It is important to further research GDF15 and reveal its specific mechanism in PCa.

In addition, suppressing or overexpressing METTL3, YTHDF1, and NMDAR2B correspondingly decreased or increased these effects, but modulation of NMDAR2B did not change the expression of METTL3/YTHDF1. rTMS can affect the polarization state of microglia and neuroinflammation by regulating the METTL3/NMDAR2B/NLRP3 signaling pathway, thereby improving NeuP.

We developed a novel predictive panel of serum m6A-related genes that could empower CRC screening and early diagnosis. METTL14, ALKBH5, YTHDC2 expression, and SOX2 protein correlate with tumor-related data and are candidates for CRC prognosis.

These findings demonstrate that YTHDF1 binds to TSC22D1 mRNA and promotes its m6A-dependent degradation. Collectively, our results suggest that EBV infection modulates m6A modification to regulate gene stability and identify the YTHDF1-TSC22D1 axis as a potential therapeutic target in EBV-associated gastric cancer.

YTHDF1 promoted resistance to oxaliplatin and 5-fluorouracil in CSCs by inhibiting apoptosis and DNA damage. In conclusion, YTHDF1 promotes stemness and chemoresistance in CRC via NOTCH1 activation. Targeting YTHDF1 is a promising strategy to improve the outcome of chemotherapy in CRC.

Higher levels of YTHDF1 and METTL3 expression in HCC tissues were associated with higher expression of PD-L1. m6A modification participates in regulating immune microenvironment of HCC, and targeting m6A may block the immune escape of HCC cells.

Furthermore, the study reveals that m6A-modified EphA10 accelerates PCa cell proliferation, invasion, and migration by activating the ERK/AKT signaling pathway. Our findings suggest that PCa stabilizes the m6A methylation of EphA10, thereby sustaining the activation of the ERK/AKT signaling pathway and accelerating cancer progression. Targeting EphA10, or the m6A methylation "writer" and "reader" proteins involved in its regulation, to inhibit this methylation process could represent a promising therapeutic strategy for PCa.

This novel protein degradation platform can address tumor recurrence after iRFA, and potentially be applied to other oncogenic targets. Furthermore, it offers a conceptual framework for treating tumors harboring traditionally "undruggable" targets.

These results collectively suggested that RBM15 accelerated trophoblast cell dysfunction via mediating m6A modification of FOSB mRNA through the identification by YTHDF1.

YTHDF1 drives HCC progression through m6A-mediated stabilization of YTHDF2, revealing their functional synergy. Their combined spatial and expression profiles offer a superior prognostic biomarker, suggesting novel therapeutic targets.

Importantly, the m6A inhibitor STM2457 reverses YTHDF1-driven oncogenic phenotypes. These findings uncover a novel mechanism by which YTHDF1 regulates c-MYC through combined effects on mRNA stability and translation, advancing understanding of m6A-mediated oncogenesis and offering new insights into epitranscriptional control of cancer progression.