STC2 (Stanniocalcin 2)

Our findings suggest that STC2 promotes anoikis resistance in CRC by regulating TGIF1 mRNA stability. STC2 may serve as a potential therapeutic target and prognostic biomarker for colorectal cancer.

These findings highlight the relevance of a dysregulation of a subset of Ca2+-signaling genes as a distinctive feature of HBV-HCC. All data generated or analyzed during this study are included in this article.

This study identified a malignant cell state in CRC that is metabolically defined and spatially limited, including liver metastases, and is characterized by elevated STC2 expression and active immune-stromal interactions. Given the interplay between metabolic reprogramming and TME remodeling, STC2+ malignant cells are a functionally significant subpopulation and a potential therapeutic target.

The identification of CA12, consistent with previous findings on its role in oncogenesis and estrogen regulation, highlights the therapeutic potential of targeting this pathway. Furthermore, the additional genes identified expand our understanding of metabolic alterations in response to estrogen signaling in breast cancer, thereby offering new avenues for mechanistic exploration and the development of potential therapeutic targets.

Moreover, we found that fucosylation of GRP78 triggers downstream ER stress signaling pathways and activates the PERK/ATF4/STC2 pathway, leading to enhanced glucose deficiency tolerance in CRC cells. Overall, our study highlights the significant role of FUT3 in the fucosylation of GRP78, which is crucial for the survival and proliferation of CRC cells in a glucose-deficient microenvironment.

By moving beyond simple mutation identification, ATHENA enables functional prediction of genomic interactions. This approach accelerates the discovery of actionable targets and provides a foundation for rational design of next-generation combination therapies in advanced prostate cancer.

The invasion and metastasis potential of gastric pain cells decreased after silencing stanniocalcin 2, suggesting that it may promote the invasion and metastasis of gastric cancer.

Molecular docking and dynamics simulations revealed valproic acid, cyclosporine, and genistein as potential therapeutic compounds with strong binding affinities to the hub genes...This comprehensive study highlights the potential of ULBP2, INHBB, and STC2 as promising biomarkers for CRC, emphasizing their roles in regulating tumor progression and immune responses. Future studies should focus on targeted therapeutic strategies that utilize these biomarkers to enhance treatment efficacy and patient prognosis.

This study elucidates the tumor-endothelial interactions mediated by STC2 and ITGA5 in smoking-associated LSCC, emphasizing their roles in tumor progression and vascular permeability. These findings suggest potential prognostic biomarkers and therapeutic targets to improve the clinical management of smoking-associated LSCC.

Furthermore, molecular docking and dynamics simulations identified ursolic acid (UA) as a stable small-molecule FOS binder, and in vitro experiments confirmed its inhibitory effects on oxidative stress and inflammation, comparable to FOS silencing or pharmacological inhibition. Collectively, our findings suggest that oxidative stress-related genes, particularly FOS, play a central role in OA pathogenesis by linking redox imbalance to immune dysregulation and chondrocyte injury, and highlight UA as a potential therapeutic candidate for OA management.

And we successfully developed a predictive model to forecast the response of CRC patients to cetuximab treatment. This study will provide valuable biomarkers for CRC prognosis and help guide more effective therapeutic strategies.

Additionally, we performed experimental research and found STC2 is significantly upregulated in CRC tissue and can promote CRC progression by regulating cancer cell invasion and proliferation. This study provides valuable insights into the oncogenic role of STC2, proposing it as a promising target for therapeutic intervention and a marker for aggressive cancer phenotypes.