WP1066

The STAT3 agonist Colivelin reverses the anti-proliferative effects of allicin, while the inhibitor WP1066 enhances these effects. These findings collectively suggest that allicin exerts its anti-inflammatory and anti-remodeling effects in asthma by targeting the STAT3/PIM1 pathway, providing a new therapeutic strategy for asthma treatment.

In contrast, after the cells were co-treated with WP1066 on the basis of co-culture with SPP1+ TAMs, MC38 cell viability was decreased, and apoptosis was increased; the levels of JAK2, STAT3, and their phosphorylation were decreased, and the EMT process was inhibited. Therefore, SPP1+ TAMs promote CRC cell proliferation and EMT by activating JAK2/STAT3 signaling pathway.

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This novel study establishes a practical and theoretical foundation for radiation electrophysiology research by demonstrating that the cellular impedance-sensing system based on microelectrode arrays can detect ionizing radiation-induced and drug-induced glioblastoma cell death in real-time.

Here we investigated the therapeutic activity of the orally bioavailable STAT3 inhibitor, WP1066, and anti-CD47 antibody using OS mouse models...This was associated with increased frequency of activated CD8+ T cells, NK cells and macrophages in the lungs and LDLNs. Our preclinical studies support further investigation of targeting STAT3 and CD47 as novel immunotherapeutic approach against OS lung metastasis.

These findings indicate that the CEACAM7/JAK2/STAT3/BST2 axis plays a crucial role in promoting NPC cell migration and underscore its potential as a therapeutic target for mitigating NPC metastasis.

The study shows the promising role of PSME2 as a therapeutic target in ESCC management. The combined inhibition of PSME2 and activated pathways ensures effective suppression of tumor growth and proliferation, thus offering a novel strategy for better treatment outcomes in ESCC patients.

The signal transducer and activator of transcription 3 (STAT3) inhibitor WP1066 is further encapsulated into COPs to form a WP1066-loaded COP (TVW)...The antitumor capacity of photodynamic immunotherapy is extensively investigated in a murine subcutaneous hepatocellular carcinoma model. This photo-immunotherapy may provide an effective combination regimen for the efficient treatment of solid tumors such as hepatocellular carcinoma.

Finally, cells with high levels of TXNIP expression displayed increased susceptibility to IL-24 and WP1066, a specific STAT3 inhibitor, suggesting possible predictive value for TXNIP. Collectively, these findings unveil novel TXNIP-dependent pathways that may contribute to breast cancer pathogenesis, enriching our understanding of this molecule's intricate role in cancer and potentially paving the way for clinical translation.

Knockdown of CXCR4 expression using short hairpin RNA, inhibition of CXCR4 signaling with AMD3100, and targeting of STAT3, a downstream effector of CXCR4, with WP1066 in DTC cells significantly diminished their self-renewal ability, tumorigenic potential, IR resistance, and Sox2 expression. Furthermore, DTC cells infected with shCXCR4 exhibited substantial tumor suppression, and the combination of IR and AMD3100 significantly reduced DTC tumor growth in a mouse xenograft model. These findings underscore the functional significance of CXCR4 as a CSC marker, highlighting its potential as a therapeutic target for malignant chordomas.

The degree of cellular uptake for the self-assembled LNPs formed by the pegylated CGKRK-lipopeptide were found to be significantly higher than that for the self-assembled LNPs formed by the pegylated RGDK-lipopeptide in MCF-7, MDA-MB-231, HEK-293 and HFF cells.  Notably, about 60% TNBCs (MDA-MB-231 cells) were killed upon treatment with commercially available potent JAK2 inhibitor (WP 1066) loaded LNPs of the pegylated RGDK-lipopeptide. Contrastingly, the same treatment killed only about 20% non-cancerous HEK-293 cells. The self-assembled pegylated LNPs described herein open the door for undertaking preclinical studies in animal models for TNBCs.

In addition, METTL14-mediated m6A modification of SOCS3 inactivated the janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) pathway, and in the METTL14-overexpressing TC cells, silencing SOCS3-induced upregulation of cell proliferation, EMT and suppression of apoptosis was reversed by JAK2/STAT3 inhibitor AG490 and WP1066. Together, we indicated that METTL14/m6A/SOCS3/ JAK2/STAT3 axis play an important role in the progression of TC.