IGF2BP1 (Insulin Like Growth Factor 2 MRNA Binding Protein 1)

The combination of KPT-8602 and IFN-γ can activate the pan-apoptotic pathway by upregulating ZBP1, thereby effectively inhibiting the growth of PCNSL. This study presented a promising new combination treatment strategy for PCNSL.

In vivo, oral administration of CA11 suppresses tumor growth by enhancing innate immunity, and is well tolerated systemically. Our findings establish CA11 as the first-in-class and orally activated telomeric G4 ligand that pharmacologically induces telomere crisis for cancer therapy.

The relationship between SERPINF1 and FTO was determined through correlation analysis, methylated RNA immunoprecipitation, luciferase, RT-qPCR, Western blotting, RNA immunoprecipitation, and actinomycin D treatment assays...Rescue experiments demonstrated that SERPINF1 overexpression reversed FTO-induced oncogenic phenotypes. These findings suggest that FTO-mediated m6A demethylation suppressed SERPINF1 expression in MM, whereas SERPINF1 overexpression inhibited tumor progression via the Wnt/β-catenin pathway.

Furthermore, we directly observe the complex in living human cells using in-cell 19F NMR for the first time. This structural information provides a platform for the design of topology-specific Z-DNA-targeting compounds and is valuable for the development of new potent anticancer drugs.

The current study recognized the most relevant genes involved in the immune system in high-grade serous ovarian cancer. The findings of this study provided a holistic understanding of the tumor microenvironment that can be used for introducing therapeutic targets.

METTL3 enhances AFAP1-AS1 stability via m6A modification recognized by YTHDF2 and IGF2BP1, which subsequently increases EGR2 expression by improving its mRNA stability. EGR2 directly activates transcription of immune checkpoint and epithelial-mesenchymal transition (EMT)-related genes. This METTL3/AFAP1-AS1/EGR2 signaling axis drives PC malignancy and immune resistance, offering potential therapeutic targets for PC treatment.

The DNA methylase inhibitor reactivated endogenous retroviruses, leading to the formation of retrovirus dsRNAs and the emergence of a new ADAR1 dependency. Our study establishes the potential of ADAR1i-124 as a future cancer therapeutic.

Additionally, METTL16-mediated m6A modification of EEF1A1 mRNA activates the m6A-IGF2BP1 axis, resulting in increased EEF1A1 protein levels and enhanced resistance to ENZ-induced apoptosis. These findings uncover a novel UFL1-METTL16-EEF1A1 signaling pathway that drives ENZ resistance, suggesting that targeting this cascade may offer a promising therapeutic strategy for overcoming ENZ resistance in prostate cancer.

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.

Dysregulation of these RBPs has been linked to aberrant Wnt signaling, contributing to various pathological conditions such as cancers or developmental disorders. This review explores the emerging landscape of RBPs in the regulation of canonical Wnt signaling, highlighting their molecular mechanism, functional implications, and potential as therapeutic targets in Wnt-driven disease.

The dysregulation of these pathways has been implicated in various human diseases, including tubulinopathies, cancer and myopathies. In this Review, we summarize the multilayered regulatory networks that control actin and tubulin abundance, highlight recent advances in autoregulatory circuits and their disease relevance, and discuss future research directions for the therapeutic targeting of cytoskeletal proteostasis.

ALKBH5 was found to demethylate the m6A of AXIN2 mRNA, reducing IGF2BP1-mediated stabilization of AXIN2 mRNA, leading to its destabilization and reduced expression, which subsequently hyperactivated the Wnt/β-catenin signaling. These results highlight the role of the ALKBH5-m6A-AXIN2-Wnt/β-catenin axis in Cd-induced stemness and proliferation in colon cancer, offering new insights into Cd-associated CRC development.