COL6A2 (Collagen Type VI Alpha 2 Chain)

These analyses identify atrophy-associated PTMs that provide refined biomarkers for fingerprinting the atrophic stimulus. Although most PTMs are stimulus-specific, P27 dihydroxylation of Lrpprc declines during muscle wasting induced by cancer, dexamethasone and aging, suggesting that this is a general atrophy marker. Experimental up-regulation of the atrophy-mimicking variant LrpprcP27A reduces muscle force compared to wild-type Lrpprc in young and old mice, suggesting that atrophy-associated P27 dihydroxylation contributes to disease-associated muscle weakness.

COL6A2 promotes ccRCC aggressiveness and modulates Wnt/β-catenin signaling in an integrin-dependent manner. These findings nominate the COL6A2-integrin interface as a potential therapeutic and biomarker axis in ccRCC.

By integrating a large amount of RNA sequencing data, we identified VCL, FLNA, TAGLN, ACTA2, COL6A2, and CALD1 as potential biomarkers for B-cell-associated bladder cancer, and experimentally verified that these markers were significantly lower in bladder cancer patients than in the normal group, and were effective in predicting the survival rate of the patients and the status of the tumor immune microenvironment. Using a combination of transcriptomic and experimental validation at single-cell and batch levels, this study provides insights into the key gene signatures of B cells from patients with bladder cancer and their roles in regulating the tumor immune microenvironment, providing new biomarkers and potential therapeutic targets for predicting patient' prognosis and immunotherapy response.

Mechanistically, COL6A2 silencing restored DCs' activation and enhanced the infiltration and function of effector immune cells. Our findings highlight COL6A2 as a key oncogenic and immunomodulatory ECM component in GBM and suggest that targeting collagen-mediated immune suppression may improve therapeutic outcomes in GBM patients.

Telotristat ethyl affects the expression of genes associated with the ECM and interferes with SI-NET-fibroblast crosstalk. Further analysis is required; however, this study represents an important step in understanding the mechanisms of telotristat ethyl when treating SI-NET patients.

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.

This study identifies COL6A2 as a powerful prognostic biomarker and a driver of ccRCC progression through EMT and immune suppression. Targeting COL6A2 holds promise for improving immunotherapy efficacy and personalizing treatment strategies, offering new hope for ccRCC patients facing limited options.

In the end, we suggested Rapamycin as the additional therapy for the advanced ccRCC. In conclusion, our study created a signature to provide opportunities for predicting prognosis and improving treatments of ccRCC.

AEBP1 is a multi-cancer drug target, underscoring its diagnostic and prognostic value in different types of cancer preventive medicine. It influences tumor growth, metastasis, and immune evasion in cancers like adrenocortical, oral, breast, bladder, gastric, colon, and ovarian by activating the NF-κB pathway and disrupting tumor suppressors. Our findings additionally identified AEBP1 as a key regulator in glioblastoma (GBM) progression, with its overexpression [log2FC = 8.207; P ≤ 0.05] linked to reduced survival [HR = 2.1; P = 4.9e-05]. Targeting AEBP1 via TGFβs and its receptors could inhibit the collagen-depositing gene COL6A2 and THBS2, a key TME modulator. Further, the hsa-miR-128-3p (AUC = 0.94) could be a potential therapeutic target to prevent the expression of AEBP1. Following an extensive review and in-depth discussion, our investigation presents a potentially promising avenue to develop small drug-like molecules and monoclonal antibodies against AEBP1 expression for ameliorating patient survival rates.

Further investigation into the potential involvement of epigenetic mechanisms in the regulation of collagen gene levels in sarcoids revealed compelling evidence of DNA methylation and microRNAs playing significant roles. The findings suggest a complex interplay between gene expression, epigenetic regulation, and the dysregulation of the ECM in sarcoid pathogenesis.

Our comprehensive study is the first report on the molecular mechanism of CVB-D against BCa, identifying GSN as a pivotal target in CVB-D-based anti-BCa therapy. We believe that our study results may help establish a theoretical basis for the possible utilization of CVB-D in cancer therapeutics.

Furthermore, qPCR and IHC confirmed elevated expression levels of the hub genes and transcription factor. We identified biomarkers, specifically TNFAIP6 and COL6A2, that have the potential to predict disease activity and aid in the diagnosis of IVDD.