In cultured cells, brevilin A reduced cell viability, induced apoptosis, suppressed migration and invasion, decreased protein levels of phospho-JAK2 (Y1007/1008) and phospho-STAT3 (Tyr705), and restrained STAT3 nuclear localization.
The interaction between EIF3F and signal transducer and activator of transcription 3 (STAT3) controlled the EIF3F-mediated increase in Snail2 expression and cellular invasion, which were specifically abrogated using the STAT3 inhibitor Nifuroxazide or knockdown approaches.
Signal transducer and activator of transcription 3 (STAT3) protein frequently overexpressed in many malignancies and plays an essential role in regulating proliferation, apoptosis, migration and invasion in cancer cells.
Furthermore, interleukin 6 (IL-6) and signal transducer and activator of transcription 3 (STAT3) expression in cells was detected by RT-PCR and western blot analysis, while CCK8, BrdU, flow cytometry, and transwell assays were used to monitor cell proliferation, apoptosis, migration and invasion, respectively.
In ¬aggressive 8505c cells, mebendazole significantly repressed migratory and invasive potential in a wound healing and transwell invasion assay and inhibited expression of phosphorylated Akt and Stat3 and reduced Gli1.
Consistently, stable short hairpin RNA (shRNA)-mediated silencing of PKM2 reversed the effects of TGF-β1 treatment, specifically, upregulation of PKM2, phosphorylation of STAT3 at Tyr705, and increased EMT, migration, and invasion.
Moreover, transient over-expression of miR-296-3p in A549 cells induced a significant decrease in the proliferation and invasion ability of A549 cells, as well as decreased expression of RABL3, MMP-2, JAK and STAT3.
STAT3-Activated Long Non-Coding RNA Lung Cancer Associated Transcript 1 Drives Cell Proliferation, Migration, and Invasion in Hepatoblastoma Through Regulation of the miR-301b/STAT3 Axis.
Additionally, STAT3 small interfering RNA significantly inhibited the migration and invasion ability of MSCs, and the expression of the STAT3 downstream targets cyclin D1 and B‑cell lymphoma‑extra large under IL22 stimulation, indicating that IL22 also promoted MSC migration and invasion through STAT3 signaling.
<b>Results:</b> The in vitro results demonstrated that lycorine induced apoptosis and cell cycle arrest and suppressed the migration and invasion by suppressing constitutive signal transducers and activators of transcription 3 (STAT3) activation through enhancing the expression of SH2 domain-containing phosphatase 1 (SHP-1) and downregulating the expression of STAT3 target proteins.
The current study investigated the effect of plasmid small interfering RNA (psiRNA)‑mediated silencing of signal transducer and activator of transcription‑3 (STAT3) on the invasion, apoptosis, and expression levels of cyclin D1, caspase‑3 and B‑cell lymphoma‑2 (Bcl‑2) in C6 glioma cells.
STAT3-induced upregulation of lncRNA DUXAP8 functions as ceRNA for miR-577 to promote the migration and invasion in colorectal cancer through the regulation of RAB14.
Signal transducer and activator of transcription 3 (STAT3) is a transcription factor involved in proliferation, metastasis, and invasion of cancer cells.
STAT3 is overexpressed and constitutively activated in TNBC cells and contributes to cell survival, proliferation, cell cycle progression, anti-apoptosis, migration, invasion, angiogenesis, chemoresistance, immunosuppression, and stem cells self-renewal and differentiation by regulating the expression of its downstream target genes.
Inhibition of STAT-1 activity by fludarabine and STAT-3 activity by Stattic also leads to a decrease in H<sub>2</sub> O<sub>2</sub> -mediated increase in HTR-8/SVneo cell invasion.
Overexpression of miR-124 remarkably reduced the expression level of STAT3 in A549/DDP cells, increased the sensitivity of A549/DDP cells to cisplatin, and inhibited the invasion and metastasis capacities of cells.
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.