MXI1 (MAX Interactor 1)

FUBP3 stabilized MXI1 to block RRAS-mediated ERK signaling. Overall, we provide evidence of an unrevealed axis FUBP3/MXI1/RRAS/MAPK in the CD8+ T cell immunity in AMKL.

These findings suggest that these genes may serve as potential therapeutic targets for the prevention and treatment of comorbidities in patients with PCOS and MetS. The identified hub genes play significant roles in the development of PCOS and MetS, underscoring the need for further research on these genes. This study offers insights into molecular interactions and potential biomarkers for early diagnosis and therapeutic targets for these syndromes. Future studies should aim to validate these findings in larger cohorts to enhance their clinical applicability.

(C) Silencing or chemical inhibition of METTL16 stabilizes MXD4 mRNA and increases its protein levels. (D) (1) Increased MXD4 proteins may counteract MYC binding with its partner MAX, thus repressing expression of MYC target genes (early event); (2) MXD4 binds to MYC regulatory regions, decreasing MYC expression (late event) and affecting AML proliferation.

Bioinformatic prediction revealed that edited miR-200b-3p gained the function to repress the expression of new targets, including tumour suppressor MAX interactor 1, dimerisation protein (MXI1), which was associated with a statistically significantly worse OS time in HGSOC patients. Our study reports the potential contribution of edited miR-200b-3p in HGSOC progression, and highlights its potential as a new therapeutic target.

This new mechanism, termed AHR-NRF2-JDP2 gene battery, may facilitate the identification of therapeutics at the reduction of reactive toxic intermediates at the nucleosome level. Identifying the AHR-NRF2-JDP2 gene battery mechanisms will enable the development of novel therapeutics for the risk assessment of oxidative stress/antioxidation, detoxification, ROS, cell death, inflammation, allergies, and cancer.

Our 3D models showed more loosely packed chromatin in cancer. This study highlights numerous possible regulatory dependencies, and the presented bioinformatic approach provides a robust framework for data dimensionality reduction, enabling the identification of key features for further experimental validation.

ESR1 expression was significantly higher in NUTM1/NUMT2B-rearranged intra-abdominal sarcomas. NUTM1/2B-rearranged intra-abdominal sarcomas herein represent an emerging entity distinct from the sarcomatous lineage at the transcriptomic level, and characterized by its overexpression of estrogen receptors, which could be an indication for another therapeutic option.

Additionally, we will summarize recent advancements in understanding the role of UBE2O in various tumors, Alzheimer's disease (AD), and metabolic diseases. Finally, we will discuss the potential of targeting UBE2O as a novel therapeutic strategy for the treatment of human diseases.

MXD3 expression level, along with lymph node involvement and methylation status, could serve as independent prognostic indicators for risk stratification and treatment decision-making in LUSC patients. Further research is warranted to elucidate the underlying mechanisms of MXD3-mediated tumorigenesis and its potential as a therapeutic target in LUSC management.

These strategies include BRD and extraterminal (BET) inhibitors, trabectedin, inhibitors of the EP300 histone acetyltransferase, and histone deacetylase inhibitors such as vorinostat. In the absence of clinical trials, the results from this review suggest that trabectedin-based or ifosfamide-based regimens, particularly in combination with doxorubicin, may offer a reasonable approach as frontline therapy for NUT sarcomas.

Among this group, MGA::NUTM1-fusion sarcomas might represent a distinctive subset. NUTM1 IHC does not reliably detect NUTM2A/NUTM2G-rearranged sarcomas.

The chromatin regulator JDP2 was found to be involved in the movement of AHR-NRF2 complexes from the dioxin response element to the antioxidant response element in the AHR promoter, during its activation in a spatiotemporal manner. This new epigenetic and chromatin remodeling role of AHR-NRF2-JDP2 axis is useful for identifying new therapeutic targets for various diseases, including immunological response, detoxification, development, and cancer-related diseases.