AZD1480

However, treatment with the JAK pathway inhibitor AZD1480 restored NK cell cytotoxicity against cancer cells. Finally, high RBM10 expression was associated with a favourable prognosis in pancreatic cancer patients, suggesting that RBM10 inhibits pancreatic cancer progression by suppressing tumour immune escape through JAK-STAT-mediated regulation of PD-1 expression in NK cells. This finding offers potential for the development of novel precision-targeted therapies in the management of pancreatic cancer.

Notably, AMD3100 (a CXCR4 antagonist) partially reversed the DEC1-OE-induced upregulation of CXCR4 and associated pro-metastatic genes...Furthermore, pharmacological inhibition of AKT (LY294002) or JAK2 (AZD1480), but not ERK (PD98059), attenuated DEC1-mediated CXCR4 upregulation, although all three inhibitors mitigated DEC1-driven migration-related gene expression. Additionally, DEC1 enhanced CXCL12 secretion from mesenchymal stromal cells and osteoblasts, amplifying the CXCR4/CXCL12 axis within the bone microenvironment. Collectively, our findings demonstrate that DEC1 promotes breast cancer (BC) bone metastasis by directly transactivating CXCR4 expression, providing a molecular basis for targeting DEC1 to prevent and treat BC bone metastasis.

In addition, we added the JAK2 inhibitor AZD1480 to explore the regulation of OTUB1 for JAK2/STAT1 pathway in GBM... Our study reveals a novel mechanism by which OTUB1 inhibits the JAK2/STAT1 signaling pathway. This contributes to a better understanding of OTUB1's role in GBM and provides a potential avenue for targeted therapeutic intervention.

VSIG4 suppresses oxidative stress, mitochondrial dysfunction, and inflammation by activating the JAK2/STAT3 pathway, which may be helpful in attenuating PD progression.

JAK2 inhibitor, AZD1480 exhibited a dose-dependent inhibition of the LIF-induced Gd-IgA1 overproduction...In summary, IgAN cells exhibit LIF-mediated overproduction of Gd-IgA1 due to abnormal signaling. JAK2 inhibitors can counter these LIF-induced effects and block Gd-IgA1 synthesis in IgAN.

Our studies discovered that lipids deposited in HDRR-LCCs were due to endogenous de novo fatty acids synthesis and exogenous lipids uptake. JAK2/p-TAT3/FASN could be used as promising targets for radiotherapy sensitization. Our study provided a new theoretical basis for studying the mechanism of radiation resistance in lung cancer.

Blocking STAT3 signaling with the JAK1/2 inhibitor AZD1480 restored PD-L1 blockade in pDCs and was associated with improved reduction of tumor burden...Our study shows that the presence of ADAs is associated with lack of antitumor responses to ant-PD-L1 blockade in a preclinical model of prostate cancer and provides additional data that will improve our understanding of ADAs against immune checkpoint inhibitors. This study also offers an approach to monitor ADA development and a platform to investigate novel approaches to target ADAs.

These results demonstrated that exosomal miR-761 modulated the tumor microenvironment via SOCS2/JAK2/STAT3 pathway-dependent activation of CAFs. Our findings may inspire new strategies for HCC prevention and therapy.

IVM accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation.

Taken together, our results suggest that IL4Rα and IL13Rα1 might be involved in the development of human gallbladder cancer cells and IL4Rα and IL13Rα1 complex/JAK2 signaling pathway could be efficient therapeutic targets for gallbladder cancer treatment.