IGF2BP3 (Insulin Like Growth Factor 2 MRNA Binding Protein 3)

Notably, combining the EBNA1-targeting PROTAC degrader EP-1215 with anti-PD-1 effectively restored IFN signaling, enhanced T-cell infiltration, and suppressed EBNA1+ tumors in humanized mice. This viral exploitation of RNA editing suggests that targeting EBNA1 could be a strategy to convert "cold" tumors into "hot" targets amenable to ICB therapy.

Key resistance pathways include: lactylated IGF2BP3 activating PCK2-NRF2 to counter lenvatinib-induced stress; ALDOA lactylation enhancing liver cancer stem cell self-renewal for chemoresistance; MOESIN lactylation in Regulatory T cells (Tregs) weakening anti-PD-1 efficacy. Therapeutically, 2-DG, AZD3965, or SIRT3 activators (reverse lactylation) restore drug sensitivity, alone or in combination. Despite limited specific detectors, lactylation is a promising target to overcome HCC drug resistance, aiding precision treatment.

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Furthermore, animal and patient-derived organoid models revealed that RBM15 enhances the sensitivity of GC to 5-fluorouracil (5-FU) chemotherapy in an ECT2-dependent manner. In conclusion, this study defines a novel RBM15/IGF2BP3-ECT2 signaling axis that regulates EMT and chemosensitivity in GC via m6A methylation, providing both mechanistic insights and a potential therapeutic strategy.

The METTL3-IGF2BP3 axis facilitates OS progression by enhancing ID1 mRNA stability and expression, highlighting its potential as a therapeutic target.

Consistent with these signatures, IMP3 silencing produced pronounced effects on lipid metabolic readouts in vitro. Together, these data identify IMP3 as a regulator of energy and lipid metabolism in cervical cancer and support its evaluation as a biomarker and potential therapeutic target.

We found that silencing CENPA significantly increased reactive oxygen species production and mitochondrial membrane potential abnormalities leading to inhibition of cell viability and proliferation and cell death, suggesting that CENPA is closely associated with the development of KIRC. In conclusion, IGF2BP3 and its downstream CENPA signature can be used for prognostic prediction of KIRC.

Collectively, our findings demonstrate that RBM15 stabilizes PFKFB4 expression in BC through an m6A-IGF2BP3-dependent mechanism and thus promotes the glycolysis and inhibits CD8+ T cell function. Targeting RBM15 sensitizes tumors to PD1 blockade and provides a promising therapeutic strategy for BC.

Based on molecular docking and molecular dynamics results, NEDD4L is believed to be a 18β-GRA biomarker, while sodium channel protein type 5 subunit alpha (SCN5A) and early growth response protein 1 (EGR1) are the potential upstream and downstream regulatory proteins, respectively. These findings provide a theoretical basis for future experimental verification.

IGF2BP3 inhibited tumor formation by promoting GSDMD stability. IGF2BP3 enhances GSDMD stability and blocks JNK signaling activation to promote eyelid BCC pyroptosis in an m6A-Dependent Manner.

In summary, our findings highlight that PCSK9 is controlled by m6A-dependent METTL3-IGF2BP3-ILF3 epitranscriptomic programs and contributes to HCC progression. The study provides a rationale for repurposing PCSK9-depleting therapeutics into a potential antitumor treatment.