FMOD (Fibromodulin)

Expression of LIGHT in atherosclerotic plaques not only correlates with markers of plaque destabilization, but is also significantly elevated in plaques from symptomatic compared to those from asymptomatic patients. These results associate LIGHT content with a rupture-prone plaque phenotype, potentially upregulated as part of a reparative response, warranting further studies.

We developed and validated a NOTCH-based prognostic model with strong predictive power in HNSCC. The NOTCH score may help assess immune status, predict treatment response, and guide personalized therapy.

This study is the first to demonstrate elevated expression of SLRPs, especially lumican and fibromodulin, in menisci of patients with MMPRT, suggesting that these proteins could serve as potential biomarkers or therapeutic targets for MMPRT treatment.

Both of which selectively decrease the viability and alter the morphologies of organoids of h SKP2 knock-in rather than wild-type mice. Our studies provide a well-characterized prostate-specific h SKP2 knock-in mouse model and offer new mechanistic insights for understanding the oncogenic role of SKP2 in shaping the prostatic microenvironment during early carcinogenesis.

FMOD downregulated Rap1B expression in thyroid carcinoma cells, and Rap1B overexpression rescue reversed the impact of FMOD on tumor progression and TAM polarization. In conclusion, FMOD exhibited an inhibitory effect on thyroid carcinoma by stimulating M1-like TAM polarization via targeting Rap1B.

Here, we show that relatively low dose breast radiotherapy X-rays are sufficient to affect the structure of collagen I in both its solubilised and fibrillar forms. Although the impact of intermediate X-ray doses on extracellular proteins was not determined, the high dose exposures which are achievable using a synchrotron source had an even greater effect on the structure of collagen I molecules and, in tendon, on the structures of many accessory extracellular matrix proteins, The unwanted side effects of radiotherapy may therefore be due to not only cellular damage but also damage to the surrounding matrix.

The ferroptosis-based risk model provides valuable prognostic insights into GBM and highlights potential therapeutic targets, emphasizing the biological significance of ferroptosis-related genes in tumor progression.

FMOD, POSTN, LTBP2, COL1A1, COL8A1, ASPN, and HBB are potential biomarkers for HF and cancer with fibrotic microenvironments. Targeting fibrosis may offer novel therapeutic approaches. Further validation and mechanistic studies are needed. This study contributes to understanding HF and cancer at the molecular level and suggests personalized treatment strategies.

Immune checkpoint genes correlation analysis showed that PD-L1 gene expression is closely related to risk score. Our study identifies a prognostic-associated risk model and provides a potential effective immunotherapy target for IDH-wildtype GBM patients.

The risk score, derived from four collagen-associated genes, could potentially act as a precise prognostic indicator for BRFS of patients. Simultaneously, our research has identified potential therapeutic targets related to collagen. Notably, PLOD3 was differentially expressed in cancer and para-cancer tissues in clinical specimens and it also was validated through in vitro studies and shown to suppress PCa tumorigenesis following its silencing.

Our results indicate that tumor-matched CAFs are unique for each tumor and affect the proliferation and the gene/protein expression of tumor cells in a distinct manner. The interaction between tumor unmatched CAFs and HNSCC cells in the tumor spheroids is associated with significant changes in the mRNA expression of CAF-specific markers and significant increases in FMOD and MMP9 in tumor cells compared to when cocultured with tumor-matched CAFs. Taken together, our results show how important the selection of CAFs is to get a reliable in vitro model that mimics the patients' tumor.

STS was found to be more likely to exhibit an immune-cold phenotype. The identified predictive genes were used to construct the nomogram with potential to identify LTS among GB patients.