TL;DR
It is suggested that METTL3 facilitated cell invasion and partially inhibited ferroptosis through catalyzing m6A methylation modification of NUPR1, validating the specific regulatory axis METTL3/NUPR1 in HCC progression.
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.
It is revealed that METTL14-dependent m6A modification of MSTRG.16 may act as an upstream driver to activate the MAPK cascade and facilitate NSCLC progression.
KIAA1429 knockdown may suppress OS progression by inhibiting m6A-dependent SLC7A11 expression, thereby promoting ferroptosis and targeting the KIAA1429/SLC7A11 axis may represent a promising therapeutic strategy for OS.
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.
This study reveals for the first time the complete molecular mechanism by which ZCCHC4-mediated UHRF1 m6A methylation promotes OS progression through epigenetic suppression of CDO1 transcription and inhibition of ferroptosis.
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