Overexpression of kinase-deficient p110 in T24 T(p85α) cells inhibited BC cell migration, but not invasion, suggesting that the inhibition of p85α on invasion is independent of PI3K activity.
The hepatocellular carcinoma cell line SMMC-7721 was treated with different concentrations of RosA (0, 20, 50, 100 μmol/L) to detect cell proliferation, cell cycle, apoptosis and invasion.PI3K pathway-specific activator IGF-1 was used to explore whether the mechanism for RosA action relates to PI3K/AKT signal pathway.Nude mice inoculated with SMMC-7721 cells were treated with different doses of RosA (0, 5, 10 and 20 mg/kg) to detect the tumor formation of cancer cells in vivo.
With increased levels of miR-214-3p and decreased levels of lncRNA PVT1 in CRC cells, the expression of phosphatidylinositol 3-kinase, putative (PI3K) and Akt was reduced, and consequently, the cell apoptosis was stimulated and cell proliferation and invasion were suppressed.
Besides, induction of the phosphatidylinositol-3 kinase/serine/threonine kinase (PI3K/Akt) pathway associated with the ovarian cancer cell migration and invasion.
Suppression of Akt with a specific inhibitor impaired the invasion ability of CD47-overexpressing cells, indicating that stimulation of the PI3K/Akt pathway served as the downstream regulator of CD47-triggered invasion.
The present study examined the inhibitory effect of BBR on the PI3K/AKT pathway in HCC and identified that BBR downregulated the expressions of phosphorylated AKT and PI3K in MHCC97‑H and HepG2 cells, inhibiting their growth, cell migration and invasion in a dose‑dependent manner.
Transcription factor SOX2 is highly expressed in invasive gliomas and maps to chromosome region 3q26 together with the genes for PI3K/AKT signaling activator PIK3CA and effector molecules of mitochondria fusion and cell invasion, MFN1 and OPA1.
Galangin induced antitumor effects in human kidney tumor cells mediated via mitochondrial mediated apoptosis, inhibition of cell migration and invasion and targeting PI3K/ AKT/mTOR signalling pathway.
In addition, PTENP1 functioned as an endogenous sponge of miR-20a to regulate PTEN expression, which mediated BC cells proliferation, invasion and drug resistance via activation the phosphatidylinositol-3 kinase (PI3K)/AKT pathway.
Cotreatment of HeLa cells with TPA plus Pra-B or LY294002 (a PI3K inhibitor) reduced cell invasion and MMP-2/-9 expression and transcriptional activity.
The presence of PIK3CA mutation was also correlated with a higher T category (p<0.001) and N category (p<0.001), as well as the presence of perinueral invasion (p<0.001) and venous invasion (p<0.001).
Our inhibitory compound named 8m inhibited Hsp90 and PI3Kα with an IC<sub>50</sub> value of 38.6 nM and 48.4 nM, respectively; it displayed improved cellular activity which could effectively induce cell cycle arrest and apoptosis in melanoma cells and lead to the inhibition of cell proliferation, colony formation, migration and invasion.
Subsequently, the expression of invasion- and migration-related factors (MMP-2 and MMP-9) and the AKT signaling pathway-related factors (AKT, p-AKT and PI3K-p85) was detected.
<b>Conclusion:</b> Our results demonstrated that miR-3691-5p contributes to HCC cell migration and invasion through activating PI3K/Akt signaling by targeting PTEN.
Knockdown of HOXC10 could inhibit the GBM U87 cells proliferation, migration and invasion, as well as decreased expression levels of key proteins in PI3K/AKT signalling pathway.
Insulin-like growth factors 1 (IGF-1) and PI3k/Akt was assayed for elaborating antagonistic mechanism of Metuzumab in migration and invasion of esophageal cancer cells.
The CD97 siRNA and expression vector was transfected to cultured human trophoblast HTR-8/SVneo, and the cell invasion as well as the protein expression in PI3K/Akt/mTOR signaling pathway were evaluated.
Specifically, we explore the roles that downstream activation of the mitogen activated protein kinase/extracellular signal-related kinase (MAPK/ERK), protein kinase C, p38 MAPK, and phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathways play in mediating colon cancer cell proliferation, survival, migration and invasion.
PIK3CA expression, cell proliferation, migration and invasion ability increased. siRNA-mediated silencing of PIK3CA in lung cancer cells decreased their proliferation and invasive capabilities, suggesting that miR-183-5p inhibited cell proliferation and invasion of lung cancer cells at least partly through downstream targeting of PIK3CA.