BGN (Biglycan)

Immunohistochemical analysis of 66 ESCC tissues revealed that high stromal BGN expression correlated with greater tumor invasion, lymphatic invasion, and shorter disease-free survival. These findings indicate that CAF-derived BGN promotes ESCC progression via TLR4-mediated signaling and modulates stromal cell behavior, highlighting its potential as a prognostic biomarker and therapeutic target.

Our findings highlight the NR2F2-BGN axis as a critical regulator of PTC progression. Targeting this axis offers a promising therapeutic strategy for PTC treatment and immune microenvironment modulation.

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.

Functional rescue experiments confirmed that BGN overexpression reverses the inhibitory effects of GLIS2 knockdown, while the Wnt/β-catenin inhibitor XAV-939 effectively blocks BGN's tumor-promoting effects. These findings establish the crucial role of the GLIS2-BGN-Wnt/β-catenin axis in regulating GC EMT and identify novel potential therapeutic targets for GC treatment.

Multivariate Cox regression analysis showed that non-surgical patients (hazard ratio &lsqb;HR]: 4.03 (1.26-12.82); P = 0.02), whose tumors presented necrosis (P < 0.001), high HS expression (P = 0.02), and low biglycan expression (HR: 2.68 &lsqb;1.16-6.18]; P = 0.02) had significantly worse overall survival rates. We concluded that the expression of GAGs and PGs in the ECM affects the plasticity of MM, modifies its phenotype, and facilitates both its progression and resistance to treatment.

Our study offers innovative perspectives on comprehending the heterogeneity within TME of TNBC, thereby facilitating the elucidation of TNBC biology and providing clinical recommendations for TNBC patients' prognosis, such as IL32high Treg infiltration, MCI evaluation, and UQCRFS1 expression.

These findings suggest that high BGN expression enhances proliferation and migration of OC cells, indicating that BGN is a potential target for treatment of OC.

Our findings reveal a previously unrecognized mechanism of exosomal BGN-mediated M2 macrophage reprogramming and CXCL10-driven oncogenic signaling in the GC microenvironment. These insights establish a novel therapeutic paradigm for GC management through disruption of tumor-macrophage communication.

BGN potentially plays a pivotal role in the progression and metastasis of ccRCC, possibly acting through the MAPK signaling pathway. Therefore, BGN holds promise as a potential therapeutic target for ccRCC.

Fibroblasts demonstrate significant heterogeneity within the CRC immune microenvironment, impacting prognosis and therapeutic responses. Key genes BGN and CERCAM emerge as potential immunotherapeutic targets, offering new strategies for precision treatment of CRC.

In conclusion, PDK1 functions as an oncogene, facilitating EOC progression by upregulating BGN and activating the NF-κB pathway. These findings may provide valuable biomarkers for the diagnosis and treatment of EOC.

BGN upregulation via SP1 causes TGM2 downregulation in gingival fibroblasts in IGF.