COMP (Cartilage Oligomeric Matrix Protein)

Mechanistically, COMP shifted transforming growth factor beta (TGFβ) signaling from canonical phosphorylated mothers against decapentaplegic homolog 2/3 (pSMAD2/3) activation toward pSMAD1/5, likely through its interaction with PMEPA1. This study suggests the COMP-PMEPA1 axis as a new driver of EMT in breast cancer models.

This study established the first comprehensive spatial transcriptomic atlas of cervical cancer, revealing unprecedented insights into tumor microenvironment organization and cellular spatial relationships.

COMP's multifunctional properties show it is much more than a biomolecular marker protein through its ability to participate in many biological processes. Further studies are warranted to fully explore the biology of this fascinating molecule, particularly in the wound repair processes.

A high mRNA expression level of AZGP1 was associated with longer disease-free survival, whereas high mRNA expressions of ASPN, COMP, RYR2, and SFRP4 were associated with shorter disease-free survival. Prostate cancer patients with genomic alterations associated with PNI may face a higher risk of disease progression after prostatectomy, highlighting the need for further prospective studies to validate these findings.

Both in vitro and in vivo experiments confirmed COMP's role in influencing PCa progression. Additionally, COMP demonstrates significant potential as a dual biomarker for both the diagnosis and recurrence prediction of PCa.

FLS are the common starting point of synovial-derived tumors, but differentiate toward different endpoints in the SC and D-TSGCT. COMP/TGFβ/SMAD signaling pathways can promote chondrogenic differentiation of synovium in SC.

COMP could serve as a prognostic biomarker and a potential therapeutic target for the treatment of GC.

Proteomics analyses indicate that COMP promotes oxidative phosphorylation and drug resistance pathways. Therefore, COMP overexpression and treatment with exogenous COMP appears to protect NSCLC cells against radiation in vitro, however treatment with inhibitors reverses COMP-mediated protection and progression.

Three hub genes (COMP, FN1, and SDC1) were identified through the PPI network, strongly linked to extracellular matrix organization (BUB1, TTK, and NUSAP1) as hub genes involved in M phase and cell cycle checkpoints. Overall, the study identified hub pathways and genes that accurately distinguish between cancer and normal samples, presenting promising new possibilities for early cancer detection and improved BC therapy.

Histopathological analysis indicates that LHP-MNs significantly preserve cartilage integrity. The study results suggest that employing polymeric MNs for transdermal delivery of LHP can be a promising treatment approach for OA, with the added benefit of excellent patient compliance.

Calpain activation was reduced in COMP-expressing cells and maintained at a lower level of activation during treatment with epirubicin...Furthermore, patients undergoing chemotherapy or endocrine therapy demonstrated significantly reduced overall survival time when tumors expressed high levels of COMP. This study identifies a novel role of COMP in chemoresistance and calpain inactivation in breast cancer, a discovery with potential implications for anti-cancer therapy.

Moreover, tumors from mice with OA demonstrated increased Ki-67 expression compared to controls (mean 24.56% vs. 6.91%, p = 0.004) but no difference in CD31, PSMA, or COMP expression (p > 0.05). OA appears to promote prostate cancer in vitro and in vivo.