ZFP36 (ZFP36 Ring Finger Protein)

The findings of this study suggest that modulating ferroptosis suppressor ZFP36 could promote cell death in rGBM via the ferroptosis pathway.

These findings uncover a zinc-dependent ZFP36L1-regulon that governs hepatocyte fate by repressing p21- and JAG1-driven senescence and NOTCH activation and highlight ZFP36L1 as a promising therapeutic target in ALD.

LCFE exerts an anti-tumor effect by activating apoptosis and autophagy processes in breast cancer cells, while having low cytotoxicity for normal breast cells, highlighting the potential of LCFE as a natural agent for cancer treatment.

This study reports that the ZFP36L2, CKS1B, PTTG1, and ITGAE genes could potentially influence breast cancer and colorectal cancer development via TCM CD8 + T cells. These four genes are putative common markers for diagnosis, treatment, and monitoring tumor response to therapies.

She was treated with azacitidine...Conclusion Our findings highlighted that, despite cytogenetic similarity, different t(2;3) translocations may exert distinct regulatory effects depending on the precise breakpoint locations. Thus, molecular characterization of MECOM rearrangements is critical for understanding disease pathogenesis and prognosis in myeloid neoplasms and may lead to the development of novel treatment.

These findings highlight the regulatory role of RBPs in ICI-induced colitis and identify cell-type-specific alterations that may drive disease progression. Importantly, we pinpoint immune checkpoint-related RBPs as potential therapeutic targets, offering new strategies to manage this clinically significant irAE.

In summary, decreased ZFP36L1 expression serves as an inherent mechanism enabling osteosarcoma to develop resistance to MTX therapy. These results highlight ZFP36L1 as a promising therapeutic target for overcoming MTX chemoresistance in osteosarcoma.

The temporal effect of 50 μM FBP on DNA breakage and the induction of apoptosis, examined by the TUNEL assay, also supports the hypothesis of FBP-mediated folate deprivation of KB cells. The evidence reported in this study sheds light on the mechanism of FBP cytotoxicity in FR-overexpressing KB cancer cells in culture and suggests possible pathways for the observation of inhibited growth for KB xenograft tumors in vivo.

These findings reveal infection-associated stromal programs that shape the immune landscape in GC and highlight CAF-directed pathways as potential therapeutic targets in H. pylori-associated GC.

According to preclinical data, RNA-based therapies targeting DLEU1, combined with nanoparticle delivery systems (such as siRNAs, antisense oligonucleotides, and CRISPR/Cas9), may be able to cross the blood-brain barrier and work in conjunction with temozolomide or ferroptosis inducers. These findings open the door to personalized treatments, focusing on DLEU1's potential in risk assessment, early diagnosis, and innovative therapies to enhance GBM outcomes.

Our integrative approach provides a catalogue of potential non-coding driver mutations and nominates ZFP36L2 as a novel PDAC driver gene with a likely tumour suppressor function.

Overall, our study reveals that Ikzf1 and Myb cooperatively bias neutrophil development against Irf8 via the lncRNA irf8-2 and Zfp36l. This study provides previously uncharacterized insights into the conserved molecular balance between neutrophil and macrophage development during myelopoiesis, with potential implications for understanding and treating myeloid disorders.