STAT3 is usually regarded as an effective molecular target for cancer treatment, and abolishing the STAT3 activity may diminish tumor growth and metastasis.
STAT3-induced upregulation of lncRNA SNHG17 predicts a poor prognosis of melanoma and promotes cell proliferation and metastasis through regulating PI3K-AKT pathway.
These data showed that CKLF1 inhibited apoptosis and promoted malignant transformation through the IL6/STAT3 pathway, and ultimately enhanced the development and metastasis of HCC.
Furthermore, compound 1 reduced the protein levels of STAT3 and its phosphorylation, as well as decreased the expression of STAT3-regulated genes involved in metastasis and survival, such as survivin and c-myc.
In A549 and H1299 cells, upregulation of ARHGAP6 inhibited tumor growth and metastasis and reduced the levels of MMP9, VEGF and p‑STAT3, while the levels STAT3 were unchanged, as demonstrated by CCK‑8, migration and invasion assays as well as western blot analysis.
Recently, many studies have shown that down-regulating the expression of inflammation by blocking nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) pathways could significantly inhibit tumor growth and metastasis.
Consistently, the expression of nuclear Tyr705-phosphorylated STAT3, an active form of STAT3, was significantly elevated in OSCC tissues compared with adjacent normal tissues, and increased nuclear staining of Tyr705-phosphorylated STAT3 was associated with metastasis and shorter overall survival.
In SW480 cells, EGF regulated HIF-1α through the STAT3 phosphorylation pathway, eventually promoting the occurrence and metastasis of colorectal cancer.
Furthermore, western blot analysis was used to quantify key metastasis- and growth-associated proteins expression <i>in vitro</i> and <i>in vivo</i>, the results suggested that CAPE-<i>p</i>NO<sub>2</sub> downregulated the proteins expression of p-EGFR, p-STAT3, p-Akt, MMP-2, MMP-9, Survivin, and key EMT-related proteins (Vimentin and N-cadherin) (<i>p</i> < 0.01), and increased the expression of E-cadherin (<i>p</i> < 0.01) <i>in vivo</i> and <i>in vitro</i>.
Epithelial-mesenchymal transition (EMT) plays a central role in promoting tumor invasion and metastasis in malignancies thorough signal transducer and activator of transcription-3 (STAT3) and nuclear factor κB (NF-κB) activation.
In summary, CYTL1 is a cytokine with tumor-suppressing characteristics that inhibits tumor metastasis and STAT3 phosphorylation in multiple types of tumors.
In renal cell carcinoma, increased STAT3 activation is associated with increased metastasis and worse survival outcomes, but clinical trials targeting the STAT3 signaling pathway have shown varying levels of success in different RCC subtypes.
Zerumbone has shown its anti-cancer effects by causing significant suppression of proliferation, survival, angiogenesis, invasion, and metastasis through the molecular modulation of different pathways such as NF-κB, Akt, and IL-6/JAK2/STAT3 (interleukin-6/janus kinase-2/signal transducer and activator of transcription 3) and their downstream target proteins.
Taken together, our data show for the first time that the feedback loop between miR-301a and JAK/STAT3 pathway may play a significant role in pancreatic cancer invasion and metastasis.
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.
Evidences from both preclinical and clinical studies have demonstrated that STAT3 plays a critical role in several malignancies associated with poor prognosis such as glioblastoma and triple-negative breast cancer, and STAT3 inhibitors have shown efficacy in inhibiting cancer growth and metastasis.
Signal transducer and activator of transcription 3 (STAT3) and its mediated signal transduction pathway play an important role in the occurrence, development and metastasis of CRC, and are related to the development of EGFR-TKI resistance in CRC.