STC1 (Stanniocalcin 1)

Our findings demonstrate that XSF inhibits MPE progression by suppressing the STC1/p65/CXCL5 axis in tumor cells, thereby reprogramming TAMs and potentiating T cell-mediated anti-tumor immunity. This study provides a mechanistic foundation for the clinical application of XSF and highlights the value of targeting tumor cell-intrinsic pathways to modulate the immune TME.

A VM-related model was constructed to assess the prognosis and therapeutic efficacy in patients with GBM, contributing to the management of GBM in clinical practice.

Orthotopic pancreatic implantation of dual-labeled STC-1 cells provides a biologically relevant and pragmatic preclinical platform that closely resembles human PNETs. This model offers valuable utility for investigating PNET biology and evaluating novel therapeutic strategies.

Bulk and spatial transcriptomic profiling of archival HIV-associated KS lesions revealed disease-specific molecular programs associated with concurrent KAD that altered tumor and microenvironment features. These findings demonstrate the heterogeneity of KS lesions that may guide future studies on KS pathogenesis and potential therapeutic targets.

Mechanistic interrogation combined NSUN2 knockout, CRISPR knock-in mutants at K692 (K692R/E), co-immunoprecipitation, RIP-seq, MeRIP-qPCR, and actinomycin-D chase to test mRNA binding, m5C modification, and stability of CDCP1/STC1... This study identifies lactate-driven NSUN2 K692 lactylation as a key driver of perineural invasion in PDAC. We define a lactate-NSUN2-m5C-CDCP1/STC1 axis that links metabolic stress-induced lysine lactylation to mRNA methylation-dependent stabilization of pro-invasive transcripts, highlighting actionable therapeutic targets to restrain neural invasion and improve patient outcomes.

Our spatial transcriptomic results from thousands of spots across multiple KS tumors indicated a correlation between high levels of STC1 and decreased expression of macrophage markers. Together, these analyses offer potential mechanisms by which KSHV infection may remodel skin tissue, inhibit immune responses against KSHV infection, and confer resistance to anticancer therapies.

This study revealed the critical role of the NETs-STC1 feedback loop in BLCA immunoresistance. Targeting this axis could simultaneously enhance efficacy and safety of immunotherapy, providing a novel translational strategy for overcoming resistance in clinical settings.

The GPSICCA score was positively correlated with stromal and immune scores, suggesting its predictive capability is related to TME involvement in ICCA. The GPSICCA model is a strong predictor of survival in ICCA patients and could help guide treatment strategies and identify potential therapeutic targets.

SIGNIFICANCE STATEMENT: The results of this study showed that fatty acids downregulate transient receptor potential ankyrin 1, a key ion channel involved in regulating the secretion of gut hormones. Furthermore, this study investigated the potential protective effects of allicin, a dietary transient receptor potential ankyrin 1 agonist, using both an in vitro secretin tumor cell-1 model and an in vivo high-fat diet-fed C57Bl/6 mouse model.

It stabilizes mRNAs like c-Myc, PD-L1, and BMI1 through reader proteins (YTHDF1/IGF2BPs), driving tumor growth, metastasis, and chemoresistance (e.g., to Cisplatin and Anlotinib). We propose METTL3 as a unifying therapeutic target to advance both regenerative dentistry and precision oncology for oral diseases. Targeting METTL3 epitranscriptomics could transform future oral therapies.

The proinflammatory environment identified by ICI status was not exclusively mediated by T-cell phenotype polarization as shown by a lack of correlation between ICI-high status and CD4+, CD4+FOXP3+, CD8+ and CD8+PD1+ T-cell density.In conclusion, we propose a ML-based algorithm to identify proinflamed HCC TMEs bearing a positive correlation with the patient's OS. Digital characterization of the TME should be validated as a tool to improve precision delivery of anticancer immunotherapy.

Furthermore, the treatment of TNF-α (an activator of the NF-κB pathway) partially reversed the inhibitory effect of sh-STC1 on the proliferation and metastasis in GBM cells. In conclusion, STC1 induced EMT thus enhances the malignancies and drug resistance of GBM cells by activating the NF-κB pathway, providing new evidence for clinical drug development in GBM.