NCOA3 (Nuclear Receptor Coactivator 3)

This study expands the overlapping morphologic and molecular spectrum of uterine neoplasms resembling uAS showing recurrent fusions (mostly ESR1::NCOA3/2), associated with mostly low-grade histology, lack of heterologous elements and paucity of stromal overgrowth. The nosological relationship of these uAS-like tumors to UTROSCT (driven similarly by ESR1::NCOA3/2 fusions) and to fusion-negative high-grade uAS remains to be verified in future studies utilizing epigenetics and other tools.

Although research on SRC3 in hormone-related cancers is relatively comprehensive, its role in non-hormonal cancers and its clinical translation potential remain insufficiently explored. Future research should examine how SRC3 inhibition affects immune signaling pathways, the tumor and immune microenvironments, tumor heterogeneity, and various aspects of clinical translation, including novel drug development and diagnostic model design.

We showed that this peptide variant binds with a stronger affinity to its target proteins than the wild-type peptide and inhibits CBP/p300 acetylase activity. This peptide variant also modulates interactomes and CBP/p300-mediated gene transcription and exhibits effective antiproliferative activity in cell-based assays.

These genetic alterations were conspicuously absent in primary tumors, suggesting their potential role in metastatic progression. Our findings represent the first demonstration of CNV-driven oncogenic evolution in UTROSCTs, particularly implicating SWI/SNF complex dysregulation in metastatic competence.

Here we present an optimized protocol for ex vivo editing and expansion of mouse Tregs (mTregs). Since a recent study demonstrated the anti-cancer potential of SRC-3 KO mTregs, we use them here as a case study.

Biochanin A exerts a significant inhibitory effect on the biological functions of HepG2 cells.

The findings suggest that RD has the potential to mitigate OP by modulating the IR microenvironment through the ER/PI3K-EP300 signaling axis. Through the integration of dose-effect weighted network pharmacology and metabolomic analysis, our study advances beyond existing descriptive research on RD and pioneers the elucidation of the ER/PI3K-EP300 axis, thereby offering a novel mechanistic explanation.

To inhibit SRC activity, natural compounds (e.g., gossypol, bufalin, verrucarin A) and synthetic small molecules (e.g., SI-2, SI-12, MCB-613) have been developed, demonstrating preclinical efficacy across several human diseases...This review summarizes current knowledge of SRC biology in benign gynecologic disorders, outlines their mechanistic roles in disease progression, and highlights opportunities for clinical translation. Targeting SRCs may ultimately represent a novel, non-hormonal, fertility-preserving therapeutic strategy in women's health.

We conclude that SCRMS with ZFP64::NCOA2/3 fusions represent a distinct, clinically aggressive sarcoma, characterized by fascicular and sometimes round cell morphology, occasional chondro-osseous differentiation and variable skeletal muscle marker expression. Recognition of this emerging subtype of SCRMS may have prognostic and therapeutic implications.

Meta-analysis of public databases also revealed aberrant levels of these proteins in ovarian and prostate cancer, and found WBP2 overexpression in the immunoreactive ovarian cancer subtype, further supporting the role of these specific protein complexes in ovarian cancer. Finally, we reviewed the challenges in chemo and hormonal therapy and posit that WBP2-positive ovarian and prostate cancer might benefit from combinational therapy involving hormonal and immunotherapy.

In conclusion, our data suggest that the UHMK1-MTHFD2 axis forms a positive feedback loop that drives PCa progression. Targeting this loop represents a promising therapeutic strategy for restraining prostate cancer development and progression.

This study elucidates the possibility that miR-137 subtly modulates metabolic genes in prostate cancer, suggesting its latent therapeutic potential as a biomarker for disease progression.