DBN1 (Drebrin 1)

In particular, the prognostic formula comprising ZHX2, SMPD4, and CHD4 using the Lasso-Cox regression model properly distinguished the BCR-free survival curves, indicating that these genes could be signatures for disulfidptosis. Decoding disulfidptosis-related data in the transcriptome would provide crucial clues for finding novel approaches to personalized cancer medicine in prostate cancer.

Overall, DBN1 was upregulated in T‑ALL, and its depletion inhibited cell migration and invasion through downregulation of GAB2 and consequent inhibition of AKT and ERK signaling cascades. The present data suggested that DBN1 could be a novel biomarker of T‑ALL infiltration, which is a novel perspective in the field of leukemia research.

Our study identifies a novel DBN1-NF2-LATS axis, and pharmacological inhibition of DBN1 represents a promising alternative intervention targeting the Hippo pathway in cancer treatment.

Mechanistically, Mg2+ attenuated the DBN1-ACTN4 interaction by decreasing DBN1S142p, which in turn enhanced the binding of ACTN4 to F-actin and promoted F-actin polymerization, ultimately reducing MMP2 expression. These findings shed new light on the crucial role of Mg deficiency in CRC progression and suggest that Mg supplementation may be a promising preventive and therapeutic strategy for CRC.

Our study suggests that drebrin-expressing T cells present an exhausted phenotype and that tumor-infiltrating drebrin+ T cells affect clinical outcomes in patients with resectable lung squamous cell cancer.

The scRNA-seq analyses confirmed that the exhausted tumor-infiltrating CD8 T cells specifically expressed drebrin. Our study suggests that drebrin-expressing T cells present an exhausted phenotype and that tumor-infiltrating drebrin T cells affect clinical outcomes in patients with resectable squamous cell lung cancer.

Interestingly, MXD3 exhibited higher predictive power for response outcomes and overall survival of immune checkpoint blockade sub-cohorts than three of seven standardized biomarkers. Altogether, our study strongly suggests that MXD3 is an immune-oncogenic molecule and could serve as a biomarker for cancer detection, prognosis, therapeutic design, and follow-up.

In vitro and in vivo results suggested that the novel lncRNA W42, which is upregulated in HCC, may serve as a potential candidate prognostic biomarker and therapeutic target in HCC patients.