YTHDC1 (YTH Domain Containing 1)

At the post-transcriptional level in the nucleus, TDP-43 promotes Ref(2)P mRNA stability by interacting with the nuclear m6A reader protein Ythdc1, which facilitates recognition of N6-methyladenosine (m6A)-modified Ref(2)P transcripts and protects them from decay. Together, these findings delineate a dual regulatory mechanism by which TDP-43 controls Ref(2)P abundance and Yki proteostasis, providing new insights into the fine-tuning of Hippo pathway activity.

Moreover, YL-5092 functionally impaired leukemia stem cells yet spared normal hematopoietic counterparts. Collectively, our work demonstrates the efficacy of a selective YTHDC1 inhibitor and suggests that targeting of m6A readers is a potential strategy in the treatment of hematologic cancers.

Targeted inhibition of YTHDC1/USP10/PLK1 axis may be an effective measure to inhibit EC progression and improve radiosensitivity.

Due to their diagnostic, prognostic and predictive value, m6A regulators have emerged as promising biomarkers in gynaecological cancers in recent years. This review highlights the role of m6A regulators and critically evaluates their biomarker and clinical potential in gynaecological cancers.

The AUC values at 3, 5, and 7 years were 0.632, 0.617, and 0.582 in GSE39582, 0.689, 0.755, and 0.951 in GSE17537, and 0.667, 0.653, and 0.649 in GSE161158. The identified T cell signature genes may function as potential therapeutic targets, while the developed prognostic model and nomogram may facilitate clinical decision-making for CC management.

Here, we demonstrate that exposure to hydroquinone (HQ), a key metabolite of benzene, upregulates RAD51 expression in human lymphoblast (TK6), consequently suppressing DNA damage...We also observed the upregulated expression of PARP1, YTHDC1, METTL3, and RAD51 in peripheral blood lymphocytes from occupationally benzene-exposed workers. Collectively, these findings suggest that RAD51 may represent a promising biomarker for monitoring benzene-induced haematological toxicity in environmentally exposed populations.

Although temozolomide (TMZ) is a cornerstone of GBM treatment, its efficacy is often compromised by inherent or acquired resistance, underscoring the urgent need to uncover molecular mechanisms, discover new therapeutic targets, and develop innovative treatment strategies. Importantly, combining the FSCN1 inhibitor NP-G2-044, with TMZ therapy resulted in stronger anti-tumor effects both in vitro and in vivo. In conclusion, the study demonstrates that nuclear F-actin formation in GBM promotes DSB repair and reveals that targeting FSCN1 with NP-G2-044 could be a promising strategy for enhancing treatment outcomes and improving the prognosis for GBM patients.

PE and BU impair mitochondrial function and energy metabolism via the m6A-modified AMPK/sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) axis, leading to excessive autophagy and cardiotoxicity. These findings reveal potential therapeutic targets for alleviating the cardiotoxicity of PE and BU.

Knockdown of either WDR3 or YTHDC1 impairs TGF-α expression and suppresses cancer cell invasiveness, whereas YTHDC1 overexpression restores the metastatic phenotype in WDR3-deficient cells. Our findings reveal a novel WDR3-YTHDC1-TGF-α axis that drives pancreatic cancer progression and suggest that targeting WDR3 may be a promising therapeutic strategy.

We further demonstrated that MEG3 expression is tightly controlled by the METTL3-YTHDC1 axis, and YTHDC1-mediated recognition of m6A-modified MEG3 is essential for the progression of RILI. These insights establish the YTHDC1-MEG3 pathway as a key molecular driver of RILI and provide a framework for the design of targeted therapies to mitigate RILI.