METTL14 (Methyltransferase 14)

The elevated expression of YWHAH indicates its role in regulating immune balance. Together these findings suggest a potential regulatory link between TNF-α, YWHAH and METTL14 in the context of NPC.

This study indicates that XFC may upregulate the expression of lncRNA MEG3 and KLF4 by modulating METTL14-mediated m6A modification of lncRNA MEG3. Through this mechanism, XFC may regulate inflammatory responses and coagulation disorders, thereby improving SPP and exerting therapeutic effects on hyperinflammation-associated hypercoagulability in patients with OA.

METTL14 demonstrates significant predictive value regarding prognosis in BC. The METTL14 has the potential to serve as a predictive biomarker and a promising target for immunotherapy.

These results provide chemical probes for exploring the role of CamA in sporulation and colonization, with potential as antivirulence agents against C. difficile infection. Our study also introduces the first chemical probes for inhibiting bacterial CcrM and human MettL5, each of which plays key roles in their respective hosts.

GPs can effectively improve glucose-metabolism disorders, reduce inflammation, and protect pancreatic tissue in T2DM rats. The mechanisms may be associated with METTL3/14 up-regulation and FTO down-regulation, leading to enhanced m6A methylation and subsequent activation of the PI3K/AKT signaling pathway. These findings provide strong evidence for GPs regulation of epigenetic m6A RNA modification and insulin-related downstream pathways, and suggest that natural compounds targeting m6A regulation may be explored in the future for metabolic disease interventions.

See also the graphical abstract(Fig. 1).

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.

CPhG alleviates oxaliplatin-induced peripheral neuropathy by dual mechanisms: reducing neuroinflammation via IL-6 suppression and promoting neuronal survival and regeneration through AKT activation and m6A-dependent epitranscriptomic regulation. Compared with duloxetine, CPhG demonstrated superior neuroprotective and anti-inflammatory effects, supporting its potential as a novel therapeutic agent for OIPN.

Our systematic machine learning analysis demonstrates that m6A regulators can effectively predict CRC prognosis and immunotherapy response. The eight-gene signature provides a practical tool for clinical risk assessment and treatment decision-making.

Targeting this m⁶A-dependent pathway may offer a promising therapeutic strategy for endometrial cancer. The online version contains supplementary material available at 10.1007/s10616-026-00898-9.

Together, the evidence supports the SAM-m6A axis as a practical framework to connect nutrient state with RNA fate decisions. It also highlights key gaps for translation, including target engagement, dose-exposure alignment, and causal validation of m6A-dependent phenotypes.

Animal study revealed that knockdown of exosomal METTL14 from AML-MSC reduced AML tumorigenesis by decreasing HOXA3 and WNT7B expression. AML-MSC-derived exosomal METTL14 facilitated AML cell growth and glycolysis by activating the HOXA3/WNT7B axis, providing a new mechanism for understanding AML-MSC-derived exosomes to promote AML progression.