Fig 1: Inhibition of AKT decreases cell growth and attenuates EMT in PTC cells. (A) MK2206 induced cell viability loss in PTC cells. PTC cells were incubated with different doses of MK2206 for 48 h, and cell viability was determined by the MTT assay (n = 6), * p < 0.05. (B) MK2206-mediated apoptosis in PTC cells. PTC cells were treated with the indicated doses of MK2206 for 48 h, were subsequently stained with fluorescein-conjugated annexin-V and propidium iodide, and analyzed by flow cytometry. Data presented by the bar graphs are the mean ± SD of three independent experiments (n = 3). * Indicates a statistically significant difference compared with control, with p < 0.05. (C,D) Inhibition of AKT reduced the markers of cell growth and EMT in PTC cells. PTC cells were treated with the indicated doses of MK2206 or transfected two different AKT siRNAs (100 nM) for 48 h. Cells were lysed, and equal amounts of proteins were immunoblotted with antibodies against pAKT, AKT, Bcl-2, Bcl-xL, caspase-3, cleaved caspase-3, PARP, E-cadherin, N-cadherin, Twist, Zeb1, and GAPDH (n = 3).
Fig 2: Forest plots showed that Twist over-expression was correlated with T stage, N stage, M stage, tumor, node and metastasis stage, and clinical stage. A: T stage; B: N stage; C: M stage; D: Tumor, node and metastasis stage; E: Clinical stage.
Fig 3: Circ_0000658 upregulates HMGA2 by downregulating miR-498 to augment EMT, proliferation, invasion and migration of BCa cells. Circ_0000658 was overexpressed or silenced in the presence or absence of miR-498 mimic or miR-498 inhibitor in T24 and 5637 cells. A The expression of circ_0000658, miR-498, and HMGA2 in T24 and 5637 cells determined with RT-qPCR; B Western blot analysis of protein expression of HMGA2 in T24 and 5637 cells; C The mRNA expression of EMT markers ß-catenin, E-cadherin, N-cadherin, Slug, Snail, ZEB1 and Twist in T24 and 5637 cells determined with RT-qPCR; D The protein expression of EMT markers ß-catenin, E-cadherin, N-cadherin, Slug, Snail, ZEB1 and Twist in T24 and 5637 cells determined with Western blot analysis; E The cell migration ability of T24 and 5637 cells measured with scratch test; F The cell proliferation of T24 and 5637 cells after circ_0000658 silencing determined with EdU assay; G The cell invasion of T24 and 5637 cells determined with Transwell assay. *p < 0.05 vs. oe-NC + mimic NC or sh-NC + inhibitor NC; #p < 0.05 vs. oe-circ_0000658 + mimic NC or sh-circ_0000658 + inhibitor NC. All cell experiments were repeated three times
Fig 4: Percent of signal strength in different grades of meningioma shown for (a) E-cadherin, (b) N-cadherin, (c) total ß-catenin, (d) NON-P ß-catenin, (e) TWIST1, (f) SNAIL & SLUG in cytoplasm, and (g) SNAIL & SLUG in nuclei.
Fig 5: SGSM2 silencing affected T47D cell adhesion and cell migration. (a) The efficiency of SGSM2 knockdown was determined by western blotting (upper panel); sc (scramble), si1, si2, and si3 SGSM2 stable cell lines were collected by G418 selection. The lower panel shows the adhesion abilities of different stable cell lines plated on three types (fibronectin, type I collagen, and type IV collagen; 1 µg/ml) of ECM proteins. Wt indicates wild-type T47D cells. (b) Cell migration abilities of four types (wt, sc, si1, si2) of T47D cells were examined with wound-healing assays; left panels show the cell migration states at 0, 24, and 48 hours. Hoechst was used to stain the nuclei. The average number of migrated cells is presented in the right panel. (c) The protein levels of E-cadherin, ß-catenin, Paxillin, FAK, SRC, Snail, and Twist were detected by western blotting in wt, sc, si1, and si2 T47D cells. ß-Actin-1, 2, 3, 4 served as the internal controls. P-values were determined with Student’s t-test; **P < 0.01. All experiments were repeated more than 3 times (n > 3).
Supplier Page from Abcam for Anti-Twist antibody [10E4E6]