DUSP1 (Dual Specificity Phosphatase 1)

Taken together, these findings offer novel insights into the role and mechanism of NAT10 in the crosstalk between cisplatin chemoresistance and immunosuppression in gastric cancer. NAT10 thus holds promise as a highly attractive target, with the potential to synergize with PD-1-based immunotherapy to reverse cisplatin resistance in gastric cancer.

Further, in vivo studies are warranted to evaluate the potential of Globo-H targeting in combination with standard treatment regimens. Overall, our work highlights the value of integrating PDO-based functional assays with molecular profiling to uncover and validate actionable targets for CRC theranostics.

Furthermore, knockdown of DUSP12 promoted, while knockdown of ZNF622 suppressed, stress-induced apoptosis. Our results support a model where DUSP12 protects cells from ZNF622 mediated stress-induced apoptosis.

We found that the PI3K inhibitor LY294002 counteracted BRIP1-driven oncogenic effects, which was evidenced by restored expression of key regulators governing apoptosis, cell cycle progression, and EMT, in addition to suppressed proliferation in GC cells. BRIP1 is postulated to function upstream of the PI3K/Akt signaling cascade. This study establishes a risk scoring model and identifies BRIP1 as a potential prognostic marker for GC.

Interaction-network analysis places DUSP15 within phosphatase-, transcriptional-, and metabolism-associated modules, consistent with scaffold-like regulatory roles. Together, these convergent structural, evolutionary, and dynamical features support a model in which DUSP15 functions predominantly as a non-catalytic adaptor, providing a mechanistic framework for its non-canonical regulation of ERK and Jak1-STAT3 signalling and its tumour-selective expression in chromophobe renal cell carcinoma.

Emerging evidence highlights that DUSP1's role is context-dependent on human cancers, including breast cancer (BC). This review synthesizes current evidence on DUSP1 biology in TNBC, with emphasis on its mechanistic involvement in chemotherapy resistance, radiation-induced immune modulation, and emerging implications for immunotherapy response.

In vivo, endothelial GPRC5B deficiency significantly accelerated tumor growth and neovascularization, phenotypes that were effectively reversed by the p38 inhibitor SB202190. Clinical specimens corroborated reduced GPRC5B expression and increased microvessel density in MetS-associated PCa. Collectively, our findings establish endothelial GPRC5B downregulation as a key molecular driver promoting pathological angiogenesis via the MKK3/6-DUSP1-p38 axis, suggesting that targeting this signaling cascade offers a promising therapeutic strategy for managing MetS-associated PCa aggression.

Persistent p38 signaling reprogrammed CAFs into an inflammatory phenotype characterized by abundant secretion of the chemokine CXCL8, which in turn enhanced metastasis of breast cancer cells. In summary, these findings identify LDHB as a key metabolic regulator in CAFs and provide insights into how metabolic reprogramming promotes the inflammatory, pro-metastatic phenotype of CAFs, highlighting activating LDHB as a potential strategy for limiting cancer metastasis.

In summary, paclitaxel induces transcriptomic and proteomic signatures of the neuronal stress response, neuroinflammation, nociception, and disturbed metabolism. These may explain, in part, the clinical phenotype of sensory loss, hypersensitivity, and neuropathic pain frequently observed in patients suffering from CIPN, but constitute pharmacologically addressable targets.

These findings suggest that mesalazine differentially modulates DUSP gene expression in normal and malignant colon epithelial cells, potentially contributing to its antiproliferative and pro-apoptotic effects through the regulation of MAPK signaling. These results provide new insights into the molecular mechanisms underlying the anticancer effects of mesalazine in colorectal cancer.

Our study demonstrates that chronic stress induces a robust, cross-paradigm PFC signature characterized by downregulation of glia/myelin and vascular pathways and suppression of immediate-early gene activity, highlighting cellular processes linking chronic stress exposure, PFC dysfunction, and psychiatric disorders.

Overall, this work highlights CEBPB as a potential biomarker for poor prognosis and points to the CEBPB-DUSP1 axis as a promising therapeutic target. Our findings also demonstrate the power of integrated transcriptomic approaches in elucidating intricate gene regulatory networks, offering a basis for new strategies to mitigate CRC progression.