Additionally, signal transducer and activator of transcription 3 (STAT3) activation was suppressed by RA in human osteosarcoma, and this suppression was restored by GSH, SP600125, and JNK-shRNA.
AK093407 is highly expressed in osteosarcoma cells and tissues, and promotes cell proliferation and viability and inhibits apoptosis of osteosarcoma cell line U-2OS via STAT3 activation.
We found that SC repressed cell viability and migration and induced apoptosis in vitro, while combined SC and erlotinib treatment enhanced osteosarcoma growth suppression by preventing feedback activation of STAT3.
Collectively, the results of this study demonstrated that BD exerts a strong inhibitory effect on tumor growth and stem cell like traits of osteosarcoma which may be partially due to STAT3 inhibition, suggesting that BD maybe a promising therapeutic candidate against osteosarcoma.
miR-340-5p gene expression in OS tissues and U2OS cells was significantly lower than that in paracancerous tissues and hFOB1.19 cells. miR-340-5p directly interacted with the 3'-untranslated region (3'-UTR) of STAT3 gene and negatively regulated its expression.
Importantly, TBL1XR1 enhanced the tumorigenicity of osteosarcoma cells via activating STAT3 signaling and TBL1XR1 expression correlated significantly with STAT3 phosphorylation in osteosarcoma.
In this study, we investigated the antitumor effect of napabucasin (NP) (BBI608), an inhibitor of STAT3 on osteosarcoma in vitro and in vivo and studied the underlying molecular mechanism.
In summary, the present studies revealed that the loss of CtBP2 constrained distant metastasis through the JAK1/Stat3 pathway in OS, suggesting that targeting CtBP2 may be a practical anti-tumor approach to prevent OS tumor progression.
The aims of this study were to determine the effect of curcumin on osteosarcoma (OS) cells due to inactivation of the p-JAK2/p-STAT3 pathway and evaluate the prognostic value of this pathway in OS.
In addition, we detected the expression of vascular endothelial growth factor (VEGF) and signal transducer and activator of transcription 3 (STAT3) in osteosarcoma cell treated with Eag1 small interfering RNAs (siRNAs).
In our previous work, we found that several canine and human osteosarcoma (OSA) cell lines, but not normal osteoblasts, exhibit constitutive phosphorylation of STAT3.
In addition, knockdown of LIF notably suppressed the proliferation and invasion of osteosarcoma via blocking the STAT3 signal pathway; in contrast, treatment with the recombinant LIF protein significantly promoted the growth and invasion of osteosarcoma through enhancing the phosphorylation of STAT3, which can be partially neutralized by the STAT3 inhibitor, HO-3867.
Our findings provide information about the underlying mechanisms of miR-204/14-3-3ζ in OS cell proliferation through the STAT3 pathway, and suggest miR-204 and 14-3-3ζ as potential therapeutic targets in OS.
<b>Conclusion:</b> These results demonstrated that the anti-OS effects of lycorine were at least partly due to the suppression of the Janus kinase 2/signal transducers and activators of transcription 3 (JAK2)/STAT3 pathway.