COL22A1 (Collagen Type XXII Alpha 1 Chain)

© 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland

This study provides insights into the molecular mechanisms underlying PAAD and establishes a theoretical foundation for the development of CAF-targeting therapeutic strategies.

Across bulk, single‑cell, and spatial layers, COL22A1 integrates molecular, cellular, and microenvironmental hallmarks of glioma aggressiveness. Its tumour‑centric expression, peri‑necrotic localisation, and independent prognostic value support COL22A1 as a robust biomarker and a tractable candidate for imaging or therapeutic strategies in treatment‑refractory disease.

Moreover, immunoblotting of BCL-2 and BAX revealed that COL22A1-OE increased resistance to apoptosis in U-87 cells. However, all these effects were reversed upon silencing of COL22A1, which suggests COL22A1 could be a promising new target for GBM therapy.

Additionally, four male-specific hub genes-DAXX, IKBKB, PDGFRA, and PPARG-were immune-related and showed sex-differential correlations with immune cell infiltration, with three of them associated with AR signaling regulation. These findings provide new insights into the molecular basis of sex differences in bladder cancer and could pave the way for more personalized and effective therapeutic strategies tailored to male and female patients.

COL22A1 plays a crucial role in dictating the malignancy of GBM through regulating the PI3K/AKT signaling pathway. Targeting COL22A1 could present a novel approach for GBM management.

Finally, kaempferol and EMD‑1204831 had an obvious inhibitory effect on the growth of GBM and sensitized GBM to cuproptosis inducers via COL22A1 in cell and animal experiments. Overall, the present study revealed a cuproptosis‑related combined regimen for GBM.

The identification of these specific genomic alterations in transformed SCLC contributes to a better understanding of the mechanisms driving this transformation. This knowledge may guide future predicting the transformation of SCLC and the development of personalized treatment strategies for these patients.

We constructed a comprehensive prognostic model related to invasion in GBM patients using genetic profiles, survival curves, immune infiltration, and radiotherapy face susceptibility. The model has good predictive ability.

COL22A1 was also positively correlated with immune checkpoints and immune-regulated genes. Our study highlights the critical role of COL22A1 in gliomas and glioma-Induced Autoimmune Encephalitis, demonstrating its strong association with poor prognosis and its significant involvement in tumor immune regulation.

Mutational profiling turned up close to 200 mutations specific for the cancer cells. Altogether, our analyses suggest that centromeric regions might hold clues to EV DNA content from pancreatic cancer, the molecular, mutational signatures thereof, and rationalizes the need for a new approach to DNA biomarker research.

A molecular risk score in treatment-naïve mCRPC state obtained either in metastatic tissue or cfDNA predicts clinical survival outcomes and offers a tumor biology-based tool to design biomarker -based enrichment clinical trials.