NID1 (Nidogen 1)

Comparative proteomic profiling further identified nidogen-1 (NID1) as a key PDAP1-repressed target. Mechanistically, loss-of-function and gain-of-function experiments demonstrated that NID1, at least in part, mediates PDAP1-modulated endothelial cell migration, invasion, and tube formation-critical processes in vascular morphogenesis.

Notably, targeted inhibition of IL-11 signaling via anti-IL-11 monoclonal antibodies effectively suppressed EV-NID1-induced liver metastasis in a murine model. In summary, our findings elucidate the mechanism underlying EV-NID1-mediated regulation of CRLM, identifying a promising therapeutic target for intervention in this disease.

Besides, the combined ETV4, LOXL2 and NID1 as prognostic markers is more reliable than any one alone. Taken together, in this study, we demonstrated that ETV4 played a critical role in CRC metastasis, and unraveled the novel regulatory axis of ETV4/LOXL2/NID1, which contributed to the malignant progression of CRC.

This suggests that loss of nidogen-1 may cause BM defects, which compromise its barrier function, thereby increasing the ability of cancer cells to extravasate and colonize the lungs. Our findings provide novel insight into cancer-stromal interplay and the role of nidogen-1 at the metastatic niche.

HIF-1/2α emerge as a pivotal drivers of AdCC progression, serving dual roles as prognostic biomarker and therapeutic target, necessitating further clinical investigation through multicenter validation studies.

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.

Significantly, the projection of RNA-seq from our tumor models to two large human melanoma datasets allowed us to discover a new gene signature associated with good prognosis and the abundance of M1-like macrophages. These results support NID1 as a novel tumor suppressor with immunomodulatory properties, and unveil the existence of key oncological drivers in the extracellular scenario.

The child received systemic chemotherapy and intrathecal topotecan as CNS prophylaxis, along with enucleation of the left eye...These processes are key drivers of cancer progression and metastasis. Proteomic analysis could be valuable in identifying proteins modulated in CSF during disease progression in RB patients, offering potential for new prognostic biomarkers.

RF ML model supported the reliability in predicting PFS for critical human urine proteins (AUC=0.89), accuracy (95%) and Bacterial proteins (AUC=0.74). To our knowledge, this is the first study to depict the predictive role of the host and bacterial urine proteome in anti-PD1-treated advanced NSCLC.

Altogether, this study highlights NID1 as a novel oncogene associated with worse EFS and metabolic LSC phenotype in AML. NID1 could serve as a biomarker and aid in further mapping LSCs to establish therapeutic strategies tackling the high relapse rates in pediatric AML.

Furthermore, we found that NID1 reduced integrin β1 stability and downregulated the transcription of HIF-1α through the FAK/Src/NF-κB p65 signaling axis, which is downstream of integrin β1. Together, the results of this study demonstrate the tumor suppressive role of NID1 in triple-negative breast cancer.

Mechanistically, our findings indicate that treatment with NID1 neutralizing antibody leads to the deregulation of hypoxia-inducible factor-1 (HIF-1α) pathway in cancer cells. Taken together, this study offers promising prospects for a new pan-cancer monoclonal antibody-based strategy by targeting the tumor-associated membrane protein NID1.