COL11A1 (Collagen Type XI Alpha 1 Chain)

In this study, we identify the tumor invasive margin as a critical determinant of immunotherapy resistance in ESCC. By defining the specific spatial markers and molecular architecture of an immune-privileged niche associated with the immune-exclusion barrier, our findings demonstrate the value of spatially resolved microenvironmental analysis. Moreover, we propose that therapeutic targeting of this boundary niche represents a promising strategy to overcome resistance in ESCC.

Background/Objectives: Therapeutic resistance remains a major obstacle in breast cancer management, particularly among estrogen receptor-positive (ERα+) tumors that initially respond to endocrine therapy such as tamoxifen... COL11A1 represents a promising, though still exploratory, biomarker of therapeutic resistance and immune modulation in breast cancer. Future prospective and subtype-specific studies are needed to clarify its diagnostic and therapeutic value and to determine whether its inclusion in immunohistochemical panels could enhance patient stratification and guide personalized treatment.

Moreover, the therapeutic effect was further enhanced by combining RMF and COL11A1 siRNA. These findings suggested COL11A1 as a potential TNBC therapeutic target, with COL11A1 siRNA combined with RMF offering a viable treatment strategy.

This model provides a valuable platform for exploring the role of key driver genes, such as TP53, in the initiation and progression of fibrosis, enabling the study of hepatic progenitor cell transformation across diverse microenvironmental contexts. As such, it holds the potential for advancing early stage drug discovery and the identification of novel therapeutic targets for the treatment of liver fibrosis.

MMP13+ myofibroblastic cancer-associated fibroblasts were associated with poorly differentiated infiltration patterns, whereas COL11A1+ myofibroblastic cancer-associated fibroblasts were associated with lymph node metastasis. These results suggest that future treatments targeting these cancer-associated fibroblasts and patient stratification based on these cancer-associated fibroblasts are warranted.

These findings establish COL11A1 as a multifaceted biomarker for BLCA, offering critical insights into diagnosis, prognosis, and therapeutic strategies. Further research should elucidate its mechanistic roles in tumorigenesis and immune regulation, with potential applications across malignancies to advance personalized oncology.

In the co-culture model of CAFs and THP-1 cells, the knockdown of GREM1 or GAS6 in CAFs significantly decreased the M2 marker expression in macrophages. In NSCLC, GREM1 and GAS6 can be valuable diagnostic targets for CAFs from primary tumors and metastatic sites; they warrant further study.

Disease-specific survival discrepancy was observed comparing breast cancer patients of the upper and lower quartile of the collagen family (COL2A1, COL11A1, COL6A1, COL6A2), THBS1 and LUM gene expression signature (log-rank test, P = 0.06). Functional proteomics suggested that collagen proteins, thrombospondin 1 and lumican are differentially expressed across breast cancer subtypes.

Dexamethasone, β-estradiol, and interleukin-1β were identified as significant upstream regulators associated with poorly differentiated gastric cancer in young females. The downstream target genes of β-estradiol included male germ cell-associated kinase, growth differentiation factor 6, endothelin 2, and collagen type XI alpha 1 chain. Our detailed RNA-seq analysis revealed that the female sex hormone, β-estradiol, plays a role in the development of poorly differentiated gastric cancer in young females.

This study provides a detailed view of the underlying molecular mechanisms in breast cancer, suggesting potential biomarkers and therapeutic targets. Its findings can contribute significantly to understanding the complexity of the breast cancer microenvironment, leading to the development of more sophisticated and targeted treatment strategies.

In parallel, differential expression of extracellular matrix genes (col1a1a,col10a1a,col11a1) and matrix remodeling enzymes (mmp9,mmp13a,mmp2) in bone and scales indicated impaired skeletal remodeling. Together, these findings highlight a pivotal role for Pth4 in the endocrine and local regulation of mineral metabolism and skeletal integrity, expanding our understanding of PTH family functions in vertebrate physiology.

These findings suggest the existence of novel molecular signatures that could improve TNBC classification, prognosis, and potential therapeutic targeting.