COL5A2 (Collagen Type V Alpha 2 Chain)

Further validation in patient samples confirmed a strong association between high PLOD1 expression and GBM, highlighting its potential as a diagnostic biomarker and therapeutic target. This robust integrative machine learning approach for biomarker discovery in GBM supports the development of more personalized treatment strategies.

Our findings suggest that osteosarcoma can rarely present with FOS gene fusions and be associated with an indolent progression, challenging the specificity of such signatures for osteoblastoma diagnosis. This discovery also raises the hypothesis of malignant transformation from osteoblastoma to osteosarcoma and underscores the necessity for diligent monitoring of FOS-rearranged bone-forming tumors for optimal therapeutic management.

This study establishes COL5A2 and the C0 OCs cluster as pivotal ECM-related signatures in OS, confirming COL5A2 drives OS proliferation through focal adhesion signaling and IGFBP3-TMEM219-mediated crosstalk-both representing promising therapeutic targets. Further investigation into ECM components is warranted to refine OS treatment strategies and improve clinical outcomes.

Protein stability analysis confirmed their destabilizing effects, while functional enrichment highlighted their involvement in key pathways driving tumorigenesis. This study identified 11 key DEGs harboring potentially pathogenic novel missense variants, highlighting vulnerabilities for precision-targeted therapies in EC.

Molecular docking further identified CCT-018159 as a candidate drug capable of markedly reducing OS cell proliferation and migration. These findings highlight the hsa_circ_0000253/miR-7/COL5A2 axis as a critical driver of OS malignancy and suggest CCT-018159 as a promising therapeutic agent, warranting further in vivo validation and clinical exploration.

The DNA methylation and EMT changes were validated through The Cancer Genome Atlas Breast Invasive Carcinoma study, which confirmed that DMGs were associated with gene expression change and that our methylation-based EMT score reliably distinguished tumors from healthy controls. Our findings support the utilization of the NAF cfDNA cfBS methylation profile for noninvasive BrC screening and pave the way for enhanced early detection of this disease.

The study underscores the prognostic relevance of ARGs in skin melanoma and their contribution to tumor immunity. Overall, our findings expand our understanding of melanoma immunogenetics, suggesting the use of angiogenesis-related genes not merely as vascular regulators, but also as immune modulators.

As a proof-of-concept, we showed that radiation-affected ECM genes are independent prognostic and predictive markers of radiotherapy benefit in MIBC. Future studies should validate these radiation-induced ECM changes in clinical samples, and explore the role of FLG in radioresistance.

The study identifies AREG as a key gene associated with sotorasib resistance in NSCLC, suggesting its potential as a biomarker and therapeutic target. Further research is needed to elucidate the mechanisms underlying AREG's role in resistance and to explore its clinical significance.

COL5A2 in LUAD induces ER stress, which is associated with elevated PD-L1 exosome secretion and macrophage PD-L1 uptake, ramping up M2 polarization in macrophages.

Additionally, elevated VCAN expression was correlated with poorer survival and a reduced response to anti-PD-1 immune checkpoint inhibitor treatment of GC. This study established a lncRNA-based risk model for predicting the prognosis of GC patients and identified a ceRNA mechanism involving AP000695.2-miR-144-3p-VCAN, presenting novel biomarkers and therapeutic targets for GC treatment.

Notably, survival was associated with MAPK1, SLC16A1, and ABCB4 in relation to patient prognosis. Our findings underscore the pivotal role of ion channels as co-factors in ECM dynamics in CRC, offering mechanistic insights into tumor-stroma crosstalk and identifying potential therapeutic targets to disrupt microenvironment-driven progression.