STAT3-induced upregulation of lncRNA ABHD11-AS1 promotes tumour progression in papillary thyroid carcinoma by regulating miR-1301-3p/STAT3 axis and PI3K/AKT signalling pathway.
Since signal transducer and activator of transcription 3 (STAT3) is aberrantly activated in hepatocellular carcinoma (HCC) and plays a key role in this tumor progression.
Abnormal activation of signal transducer and activator of transcription 3 (STAT3) is complicated in the tumor progression of multiple cancers including human head and neck squamous cell carcinoma (HNSCC) and, therefore, serves as a potent therapeutic target.
Taken together, these results indicate that TNF-α and IFN-γ pretreatment effectively inhibited the repair ability of MSCs and accelerated inflammation and tumor progression involving NF-κB/STAT3 pathway and angiogenesis-related factors.
Excessive STAT3 activation within cancer cells and cells of the tumour microenvironment can be viewed as a neoplastic mimic of an inflammation-driven repair response that collectively promotes tumour progression.
Hepatic Stress Response in HCV Infection Promotes STAT3-Mediated Inhibition of HNF4A-<i>miR-122</i> Feedback Loop in Liver Fibrosis and Cancer Progression.
Newly formed NETs directly upregulated the Toll-like receptor 9 (TLR9) pathways in DLBCL and subsequently activated NFκB, STAT3, and p38 pathways to promote tumor progression.
In addition, gene knockdown and RNAseq were used to investigate molecular mechanisms through which STAT3 regulates tumor progression and the survival in lung cancer.
Accumulating evidence indicates that these tolerogenic properties are highly regulated by the constitutive and persistent activation of the oncogenic signal transducer and activator of transcription 3 (STAT3) protein, which impairs anti-tumor immunity and enhances tumor progression.
Cancer mutations and epigenetic alterations may alter the balance between pro-oncogenic and tumor suppressor activities associated with STAT3/5 signaling, explaining their context-dependent association with tumor progression both in human cancers and animal models.
In this review we will focus on the role of STAT3 and its regulation, e.g. by phosphorylation or acetylation in immune cells and how it might impact immune cell function and tumor progression.
In conclusion, our data suggested that for HSCC patients, AIM2 and p‑STAT3 expression detected via IHC could serve as a biomarker to predict tumor progression and as an independent prognostic factor.
This TRF2-dependent regulation facilitated the recruitment of MDSCs, their activation via the TLR2/MyD88/IL-6/STAT3 pathway leading to the inhibition of natural killer recruitment and cytotoxicity, and ultimately tumor progression and metastasis.
Our results imply a mechanism in which quantitative differences of STAT3 Tyr705 phosphorylation, as compared with other activation modes, direct discrete outcomes in tumor progression.
Signal transducers and activators of transcription-3 (STAT3) is constitutively activated in MB where it functions as an oncoprotein, mediating cancer progression and metastasis.