Functional-blocking monoclonal antibody against integrins alpha(v)beta3, but not alpha2 alpha3, alpha4 alpha6 beta1, beta4 or alpha2beta1, inhibited the IGF-1-stimulated invasion and proliferation in cervical cancer cells. alpha(v)beta3 integrin modulated IGF-1R phosphorylation by altering the rate of Src homology 2-containing phosphotyrosine phosphatase (SHP-2) recruitment to the activated IGF-1R.
Here, we show: 1) there was lower proliferation in the AS syndecan-1 cells compared to controls (parental HRA cells and S syndecan-1 cells) when cells were incubated with HB-GFs (HB-EGF, HGF, or FGF2); 2) transfection of HRA cells with a syndecan-1 AS ODN enhanced the increase in HB-GF-dependent invasiveness; 3) in contrast, IGF-I stimulated cell proliferation and invasion, irrespective of whether cells were transfected with the AS syndecan-1 gene; 4) IGF-I stimulated ERK1/2 activation and uPA expression in both the control and AS cells, whereas the net effect of the reduction of syndecan-1 is to shift the HB-GF dose-response curve to the right; 5) the AS cells reduced activation and up-regulation of ERK1/2 phosphorylation and uPA expression, respectively, in response to HB-GFs; and 6) in comparison with early stage ovarian cancer tissues, there was a 3-fold decrease in syndecan-1 mRNA levels in advanced stage tissues.
The effect of LTC (IC50) combined with siRNA on suppressing MG63 cells proliferation, migration, and invasion was more obvious, while the effect of LTC (IC50) combined with pEABE-bleo IGF-1R transfection was less significant (P<0.05).
Furthermore, CD8-IGF-IR caused cells to undergo an epithelial-to-mesenchymal transition (EMT) which was associated with dramatically increased migration and invasion.
However, insulin-like growth factor-1 (an activator of PI3K/AKT signaling) reversed the effects of allicin on cell invasion and expression of MMP-2, MMP-9, TIMP-1 and TIMP-2.
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.
In addition, shikonin also inhibited the expression of p-PI3K and p-Akt to attenuate cell migration and invasion and MMP-2 and MMP-9 expression in both cell lines, which could be reversed by the PI3K/Akt pathway agonist, insulin-like growth factor-1 (IGF-1).
Next, Hep3B cells were pretreated with insulin-like growth factor-1 (IGF-1) (an activator of AKT), and then transfected with CTRP6 siRNA, and the cell vitality, apoptosis, migration, and invasion were measured again.
The in vitro results showed that compared with the blank group, cell proliferation, migration and invasion were suppressed, mRNA and protein levels of IGF-1, PI3K, Akt, VEGF, bFGF and IL-8 were reduced, and cell apoptosis was enhanced in the miR-135a mimics and IGF-1 siRNA groups.
Insulin-like growth factor binding protein 2 (IGFBP2) binds insulin, IGF1 and IGF2 in circulation, thereby modulating cell survival, migration, and invasion in neoplasms.
Knockdown of IGF-IR results in a decrease of phospho-AKT and phospho-p70s6k, as well as decreased migration and invasion of MDA-MB-231Br brain-seeking cells.
The normalization rates of growth hormone and IGF-1 secretion, respectively, depend on tumour-related factors such as size, extension, the presence or absence of invasion and the magnitude of IGF-1 and growth hormone oversecretion.
Vitreal EGF and serum IGF-1 levels were significantly higher in patients with scleral invasion (15.72+/-29.13, 199.01+/-154.01 pg/ml, respectively) when compared with the patients without invasion (0.56+/-1.05, 33.01+/-36.52 pg/ml) (P=0.03 and 0.015).
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.
We hypothesized that ADAM-10 mRNA and protein may be regulated by growth factors such as 5alpha-dihydrotestosterone, insulin-like growth factor I, and epidermal growth factor, known modulators of PCa cell growth and invasion.