SSRP1 (Structure Specific Recognition Protein 1)

Ectopic SSRP1 expression abrogated AACOCF3-induced phenotypic alterations, concurrently suppressing IFN-α/β signaling. Collectively, these results provide evidence that AACOCF3 exerts its anti-proliferative effect by targeting SSRP1, which leads to the activation of the IFNα/β pathway, thereby underscoring its therapeutic promise for the cPLA2-negative patient subpopulation.

ZUP1 facilitates olaparib resistance in TNBC by stabilizing PARP1 and enhancing DNA damage repair. Pharmacological inhibition of ZUP1 with procyanidin C1 represents a promising therapeutic strategy to overcome olaparib resistance in TNBC.

Drug sensitivity analysis identified four promising therapeutic compounds-PD-0325901, Bryostatin-1, ATRA, and Roscovitine-with potential clinical utility for ESCC treatment. The findings of this study offer clinically relevant insights for prognostic stratification and characterization of the immune microenvironment in ESCC patients. Moreover, these results provide novel perspectives that may contribute to the development of more effective prognostic tools and targeted therapeutic strategies for ESCC management.

This molecular rewiring promotes fatty acid oxidation, confers resistance to ferroptosis, and importantly, drives docetaxel (DTX) chemoresistance. In DTX-resistant NSCLC cell lines, patient-derived organoids, and Nude mouse xenograft tumor model, antisense oligonucleotide-based targeting of SNHG3ED effectively restored DTX sensitivity and suppressed tumor growth. Our findings demonstrate that SNHG3 c.1746 A > I editing serves both as a novel prognostic biomarker for NSCLC and as a mechanistically defined therapeutic target to overcome DTX resistance, which offers a potential therapeutic target to improve DTX efficacy.

AEBP1 knockdown reduced the protein levels of GLI1, and treatment with the GLI-specific inhibitor GANT61 induced markers that were not suppressed by the forced expression of AEBP1. These findings suggest that AEBP1-mediated GLI1 expression reduces the FACT complex dependency of bladder cancer cell survival.

These findings underscore the therapeutic promise of traditional Chinese medicines in managing dormant cancer cells. Future studies should identify active compounds and validate mechanisms in advanced models.

Quinacrine disrupts SLC3A2-mediated arginine transport by targeting SSRP1. Combining quinacrine with histone deacetylase inhibitors is a promising therapeutic strategy for PTCL.

Lastly, we show that human and murine paramyxovirus target SUMOylated Spt16 proteins for degradation in human and murine cells utilizing a conserved N-terminal motif in their accessory "C" proteins. Collectively, our study illustrates that DNA and RNA viruses have independently evolved diverse mechanisms to antagonize SUMOylated host Spt16 proteins, underscoring the physiological importance of the FEAR pathway to antiviral immunity.

Increased expression of structure specific recognition protein-1(SSRP-1) protein supports the increased rate of chromatin remodeling in breast cancer cell lines. The results may lead to developing a new strategy for diagnosing TNBC patients.

Notably, SP-A exhibits strong synergistic effects when combined with the proteasome inhibitor bortezomib...In the case of drug intervention, SP-A attenuates the binding of SSRP1 and USP10 by inhibiting protein interactions between TRIB3 and SSRP1 and promoted SSRP1 protein degradation, leading to significant inhibition of MM development. Visual abstract created with Biorender.

Furthermore, we validated the localization of several host proteins to viral RCs using immunofluorescence microscopy and immunoblotting and identified cellular HMGB1 as a proviral factor late during infection. These findings represent the first analysis of the proteomes of isolated RCs and not only enhance our understanding of nuclear organization during infection but also shed light on the complex interplay between viral and host factors within RCs.

Overall, eosinophil infiltration in HCC is significantly correlated with patient survival. The risk assessment model based on eosinophil-related genes serves as a reliable clinical prognostic indicator and provides insights for precise treatment of HCC.