TBK1 (TANK Binding Kinase 1)

Endothelium-specific TBK1 knockdown or GSK8612 treatment inhibits EndMT and plaque formation. Safe TBK1 inhibitors could be developed into effective agents for the treatment of atherosclerotic vascular disease.

Here, a novel combination therapy consisting of the calcineurin inhibitor cyclosporine A (CsA) and the flavone-naphthalimide-polyamine derivative 6c was identified...Finally, combination of CsA and 6c suppressed tumor growth and pulmonary metastasis in vivo. Overall, our study suggests a novel synergistic treatment combination with a comprehensive mechanistic exploration, demonstrating that it is a promising strategy for HCC treatment via targeting RIG-I-like receptor signaling.

The relative expression of PRKCQ and its associated signaling components suggests their critical role in breast cancer progression. These molecules, especially PRKCQ, may serve as potential biomarkers for early detection and prognosis, as well as targets for therapeutic intervention following further validation.

Inhibiting NMD enhanced the effectiveness of immune checkpoint blockade (ICB) therapy in CRC. By uncovering the biological relevance and translational potential of targeting NMD to reconstruct TME, this study highlights its promise as a treatment strategy for CRC.

Taken together, our results demonstrated that AOH1996 suppressed tumor growth, eliminated cancer stem cells (CSCs), and synergistically enhanced the efficacy of anti-PD1 immunotherapy in HNSCC.

The TBK1-associated oncogenic mechanism is prominent in UTUC patients with preexisting ESRD. Withaferin A demonstrates preclinical promise as a therapeutic candidate targeting this mechanism in UTUC patients with compromised renal function.

scRNA-seq validated hub gene expression profiles. This study identified four ferroptosis hub genes in NPC, offering insights into its molecular mechanisms and potential diagnostic/therapeutic targets.

Flow cytometric analysis indicated a significant decrease in M2 macrophages (F4/80+CD206+) in the intervention group, with no substantial change observed in the proportion of M1 macrophages (F4/80+CD86+). Combined administration of amlexanox and anti-MCP-1 mAb inhibited tumor cell proliferation, promoted apoptosis, and reduced infiltration of tumor-associated M2 macrophages, thereby contributing to suppression of tumor progression in the LLC murine model.

Echinacoside regulates abnormal mitochondrial fission via the TBK1/Drp1 pathway, reducing the proliferation and inflammatory response of MH7A cells.

The combination of CMTM4 inhibition and anti-PD-1 treatment shows promising antitumor efficacy against CC. These findings offer novel insights into the tumor microenvironment and have the potential to inform the development of innovative immunotherapy approaches for CC.

This study presents a promising approach for treating chemo-resistant CRC by combining OVs and TBK1i.

Our results identify a ready-to-use small molecule compound for STING activation, reveal the underlying molecular mechanism through which ABT-199 activates the STING signaling pathway, and provide a theoretical basis for the use of ABT-199 in cancer immunotherapy.