STX4 (Syntaxin 4)

Functional enrichment analysis further linked the ABCC1-centred phospho-network to carcinogenesis, cell-cycle regulation, and drug resistance pathways, highlighting its systems-level role in cancer biology. From a translational perspective, our findings identify phosphosites within the ABCC1 linker domain as actionable regulatory nodes that may be exploited to modulate transporter function, offering potential strategies to overcome chemoresistance.

In lens cells, the eHSP90α's secretion undertakes secretory autophagy pathway through interacting with TRIM16 and SEC22B. TGF-β2 elevates eHSP90α secretion through upregulating secretory autophagy pathway, which in turn promote TGF-β2-induced lens epithelial cells' differentiation to lens fiber cells.

We provide a genome-wide drug target prioritization list for breast cancer derived from integrated large-scale omics data.

We demonstrated for the first time that STX4, an important regulator of OC progression, was associated with the growth and metastasis of OC cells through correlations with EMT, MMP2, and CCND1, suggesting its potential as a new therapeutic target for OC.

TRIM16 knockdown reduced autophagosomes at the plasma membrane and decreased IL6 secretion from CAFs. These findings uncover key molecular components involved in autophagy-mediated IL6 secretion in CAFs and suggest potential therapeutic targets for HNSCC.

In the present study, we have established two models of drug-induced senescence in vitro using DNA damaging chemotherapeutics, namely etoposide (0.75-5 µM) and cisplatin (1.25-5 µM), and ten skin cancer cell lines, both melanoma (n = 8, A375, G-361, MM370, SH-4, SK-MEL-1, MeWo, MM127, RPMI-7951) and non-melanoma (n = 2, A431, MCC13), to investigate the levels of 97 cell surface markers. We document that integrin α1 can be considered as a novel marker of drug-induced senescent melanoma cells. Thus, we postulate that new integrin α1-based targeted therapies can be designed and tested against drug-induced senescent melanoma cells.

Simultaneous detection of FUT8, STX4, and calpain2 expression in ovarian tumor tissues provides valuable diagnostic insights for malignant ovarian tumors.

To further characterize SA and pinpoint its involvement in neuroinflammatory processes, we studied SA-relevant protein interaction networks in mouse brain, microglia and human postmortem brain tissue from control subjects and Alzheimer disease cases. We demonstrate that SA regulates neuroinflammation-mediated neurodegeneration via SKA2 and FKBP5 signaling.

In summary, the gene signature related to exosome formation and secretion could reliably predict patients' chemosensitivity and ICB treatment response, which providing new independent biomarkers for the treatment of CRC.

Our findings suggest that patients presenting higher STX4 levels may exhibit enhanced responsiveness to immunotherapy and higher sensitivity to the medications axitinib and everolimus. Finally, we propose STX4 expression assessment as a novel approach to predict patient response to respective immunotherapies and targeted treatments, hence potentially improving patient outcomes.

This study contributes to characterizing cross-presentation of two promising Ag delivery systems and adds to the discussion about the role of Sec22b/Stx4 in related pathways. Our data point toward SNARE protein redundancy in the cytosolic pathway of cross-presentation.