JUN (Jun proto-oncogene)

This study is the first to integrate bibliometric and bioinformatics methods, revealing the macro-level trends in OP-ATG research and the molecular mechanisms underlying OP-LP crossover. It successfully identified five key OP-LP targets, providing a new perspective for understanding OP mechanisms and developing targeted therapies.

The partial reversal of this effect by the MEK/ERK inhibitor PD98059 confirmed the role of this pathway in the transcriptional control of VEGFA...Integrative bioinformatic analyses of GEO and TCGA-LIHC datasets supported these experimental findings, revealing hypoxia-associated upregulation of VEGFA, positive correlations between hypoxia scores and VEGFA/HIF1A expression, and context-dependent associations between ADAMTS1 expression, hypoxia signaling, and angiogenesis-related gene networks. These results identify ADAMTS1 as a hypoxia-responsive gene regulated through VEGFA-driven convergence of MAPK and PI3K/AKT signaling on a transcriptionally complex promoter, providing mechanistic insight into hypoxia-associated extracellular matrix remodeling in cancer.

Ferroptosis was induced with erastin, and its inhibition was achieved with ferrostatin-1...Our findings demonstrate that GPR137 deletion promotes ferroptosis in SHH-MB cells by inhibiting the Wnt/β-catenin signaling pathway. This reveals a novel regulatory axis in MB and suggests that targeting GPR137 could be a promising therapeutic strategy for SHH-MB.

Notably, ATF2 mutants incapable of nuclear import can localise to the nucleus when co-expressed with c-Jun, indicating that c-Jun can facilitate ATF2 nuclear import via heterodimerisation. Together, these results establish that ATF2 enters the nucleus through IMPα recognition of two basic clusters and highlight the redundancy and complexity of ATF2 nuclear trafficking mechanisms.

The findings suggest that Codonopsis pilosula may elicit antidepressant effects through a multi-component, multi-target, and multi-pathway approach, laying a foundation for further exploration and clinical utilization of Codonopsis pilosula in the prevention and treatment of depression.

Our findings identify SOX21 as a key regulator that prevents GPC malignancy by targeting and repressing an AP-1-driven, tumor-promoting gene expression program. These results highlight SOX21-regulated pathways as promising therapeutic targets for GBM.

NPM1 acts as an oncogenic driver in colorectal cancer by activating the AKT/mTOR signaling pathway. Elevated NPM1 expression highlights its potential as a diagnostic, prognostic, and therapeutic biomarker in CRC.

Following enzalutamide (ENZ) treatment, GSTA1 expression is inhibited...TNFRSF13B induces c-Fos expression, forming a transcriptional complex with c-Jun, thereby regulating chromogranin A (CHGA) and promoting the neuroendocrine phenotype. Our study suggested that GSTA1 deficiency leads to elevated ROS levels and activation of TNFRSF13B and c-FOS, which subsequently transcriptionally regulate CHGA and ultimately drive neuroendocrine differentiation in PCa.

These results demonstrate that tgfb2b plays a significant role in ovarian differentiation and development. Further functional and molecular studies on the interplay between tgfb2b and the foxl2-cyp19a-esr axis will help elucidate the regulatory network underlying sex development in teleost.

Cell experiments showed that sodium hydrosulfide (NaHS), a donor of H2S, prominently inhibited cell proliferation, promoted cell apoptosis for CRC, and downregulated the expression of MAPK1, MAPK3, AKT1, and JUN. Taken together, this study elucidates the possible genes and therapeutic mechanisms underlying exogenous H2S intervention in CRC, thereby laying a foundation for the further development of H2S-based therapeutic strategies in CRC management.

Non-viral c-JUN+B7-H3 CAR T cells show enhanced killing of both SCLC cells with low antigen density and thoracic SMARCA4-deficient UTs, providing a platform to address these highly aggressive entities. We also provide evidence that good manufacturing practice (GMP) clinical-scale manufacturing is feasible for c-JUN+B7-H3 CAR T cells.

This orderly cell cycle progression enhances cell proliferation and improves the hematopoietic function of myeloid cells after 5-FU chemotherapy. Consequently, BBD restores the ratio of peripheral T-cell subsets, corrects the imbalance of Th-cell subsets, and enhances the activation and proliferation functions of CD4+T cells and CD8+T cells, ultimately rectifying the dysregulated immune homeostasis of the organism.