KCNN4 (Potassium Calcium-Activated Channel Subfamily N Member 4)

Moreover, KCNN4 knockdown suppresses tumor growth and synergizes with enzalutamide in xenograft models, underscoring the therapeutic potential of targeting the p300-KCNN4 axis. Collectively, our findings reveal a previously unrecognized epigenetic regulatory mechanism coupling p300-mediated acetylation to potassium channel stability, providing a promising therapeutic strategy to overcome chemoresistance in advanced prostate cancer.

This study identified three LUAD subtypes with distinct immune characteristics and constructed a seven-gene prognostic model. This model correlates with immune checkpoint and chemotherapy sensitivity, providing new targets and strategies for clinical diagnosis and treatment.

These findings enhance our understanding of the molecular mechanisms by which BPA induces ccRCC and highlight potential targets for therapeutic intervention, particularly in endocrine and immune-related pathways. This underscores the need for collaborative efforts to mitigate the impact of environmental toxins like BPA on public health.

Additionally, high expressions of the 10-NMRGs were noted in the mesenchymal GBM subtype. Collectively, our analysis highlights the potential use of the 10-NMRG signature to stratify the high-risk GBM group with a strong association of immunomodulation and tumour-associated hallmarks that can contribute to the poor survival outcomes.

Drug sensitivity analysis revealed that tyrosine kinase inhibitors (e.g., ceritinib, imatinib) potently inhibited cancer cell lines in the high PC score group, while inhibitors like acalabrutinib were effective in the low PC score group. Expression of hub genes in KIRC patients was validated using a local cohort and single-cell sequencing. We identified key genes regulating PC infiltration in KIRC and proposed a predictive model that effectively identifies high-risk KIRC patients.

Single-cell RNA sequencing demonstrated that CACNA1C was expressed in fibroblasts and myofibroblasts, PIEZO1 was expressed across all five cell subtypes, and TRPV4 was expressed in fibroblasts and monocytes or macrophages. This study initially identified unique molecular subtypes and key genes for patients with OC from the novel angle of MICs.

Molecular docking results indicated stable interactions between IL-10 and BIRC3 with the constituents of LJF. This study highlights LJF's anti-inflammatory potential in restoring the Treg/Th17 balance and regulating cytokine expression in COPD.

Finally, a VTE-related risk score model was constructed, indicating better outcomes in the low-VTE risk score group. This study demonstrated that VTE is closely associated with BC development and identified potential molecular pathways linking the two conditions.

Importantly, modulation of the activity of KCa channels reduced the proliferation and migration of GBM cells and suppressed glioma progression both in vivo and in vitro cell models for GBM. Herein, we aim to review how modulation of the activity of KCa channels impacts tumor development in terms of proliferation, cell death, invasion, metabolism and immune system in GBM.

The landscape of cytokines, checkpoint ligands and receptors uncovered Mrc1, PD-L1, TIM-3 or B7-H3, among the immunotherapy targets that can be addressed in this model. The comparison with human GBMs unveiled crucial similarities with TMEMed GBM, the most frequent subtype.

Several MRGs are aberrantly expressed in KIRC, from which we screened 23 genes and constructed a MRGs prognostic risk model that can effectively predict the prognosis of KIRC patients and provide a new foundation for personalised diagnosis and treatment of KIRC.

Among the differentially expressed genes, transcript levels of several genes, including Itgb2, Rftn2, and Kcnn4, were significantly higher in all cell populations that comprised this lineage compared with all cell populations from the other three lineages. In conclusion, we have derived an aggressive, highly brain metastatic B16 variant associated with leptomeningeal disease by serially passaging cells in vivo.