TL;DR
This study reveals post-transcriptional regulation of METTL3 by miR-338-5p by confirming a functional miR-338-5p/METTL3/m6A axis in TNBC and targeting this distinct regulatory axis represents a promising therapeutic strategy for TNBC.
Triple-negative breast cancer (TNBC) has a high incidence of metastasis and limited therapeutic options. Here, we identify a multimodal and targetable miR-342-E2F network that regulates metastatic outgrowth in TNBC. Through integrating clinical and experimental datasets, we uncover miR-342 as a suppressor of TNBC metas...
A novel METTL3/ELF1/GPX4 axis through which METTL3 promotes TNBC growth by regulating oxidative stress and ferroptosis-related markers is suggested, providing a basis for further investigation of this pathway in the context of TNBC biology and therapeutic development.
A METTL3-m^6A-IGF2BP2 axis maintains MTFR1 expression to drive glycolytic reprogramming and CRC progression, and represents a prognostic biomarker and a potential therapeutic node linking epitranscriptomic regulation to metabolic adaptation in CRC.
Findings unveil a dual-axis regulatory mechanism in SKCM pathogenesis and position circ17399 as a promising diagnostic biomarker and actionable therapeutic target for melanoma intervention.
The reduction in ANP32E protein expression following miR-548f-3p restoration, together with computational, single-cell, and clinical expression evidence, supports ANP32E as an expression-responsive candidate downstream effector of miR-548f-3p in TNBC.
These findings establish METTL14 as a central pharmacological target whose inhibition suppresses the Wnt9a/β-catenin pathway, enhances radiotherapy and anti-PD-1 efficacy, and reduces CSC-driven progression in NSCLC.
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