NID2 (Nidogen 2)

Western blotting analysis showed activation of Akt and Bcl-xL in NID2-overexpressed cells. Our results show that NID2 is a promising prognostic marker in glioma.

Intravital imaging revealed improved vascular patency in live NID2-depleted tumors, with enhanced response to gemcitabine/Abraxane. In orthotopic models, NID2 CRISPRi tumors had less liver metastasis and increased survival, highlighting NID2 as a potential PDAC cotarget.

We demonstrated that NID2 is a potential key factor in the collagen phenotype, is involved in fibroblast activation in melanoma, and forms a barrier to limit the proximity of CD8+ T cells to tumor cells. We clarified the adverse effects of collagen on melanoma patients and identified NID2 as a potential therapeutic target.

3D invasion assays revealed that depletion of CAF-derived NID2 significantly impeded the invasion of cancer cells and enhanced standard-of-care Gemcitabine/Abraxane chemotherapy. In conclusion, temporally resolved LC-MS/MS proteomics of clinically relevant mouse models of pancreatic cancer has revealed NID2 as a new stromal co-target in this aggressive disease. Future work involves pharmacologically targeting NID2 using domain-specific blocking antibodies to effectively target NID2 in the pancreatic tumour microenvironment.

The high specificity is maintained in salivary and serum samples, facilitating accurate and non-invasive prognostication of HNSCC. The relatively lower sensitivity of NID-2 methylation may be overcome by analysing it along with a panel of multiple biomarkers such as HOX-A2 and YKL20.

Moreover, KEGG analysis revealed that the extracellular matrix-receptor (ECM-receptor) interaction pathway is mainly involved in PC. MiR-153 is up-regulated in PC tissues and may play an important role in aggressive PC by targeting potential target genes.