phos akt1  (Cell Signaling Technology Inc)

Journal: Drug Design, Development and Therapy

Article Title: Combination of Sodium Cantharidinate with Cisplatin Synergistically Hampers Growth of Cervical Cancer

doi: 10.2147/DDDT.S282777

Figure Lengend Snippet: SC inhibits the growth as well as drug resistance of CC cells in vivo. ( A ) process diagram; ( B ) growth curves of tumors; ( C ) weight of tumors; ( D – G ) immunohistochemical staining of the number of positive cells for KI67 ( D ), PTPN1 ( E ), phos-PI3K ( F ), and phos-AKT1 ( G ) in xenograft tumors; ( H ), the proportion of apoptotic cells in tumors determined by TUNEL staining. The experiments were repeated at least three times. N = 6. The data are expressed as the means ± SD of three experiments. Statistical analysis was performed utilizing the one-way (panel C – H ) or two-way ANOVA (panel B ) test combined with Tukey’s test. ** p < 0.01 vs mice injected with Caski-1 + PBS; ## p < 0.01 vs mice injected with Caski-1/R + PBS.

Article Snippet: The membranes were sealed with 5% skim milk for 90 min at ambient temperature, followed by incubation with primary antibodies (1:1000 dilution) to PTPN1 (MABS197, Millipore), phos-PI3K (ab182651, Abcam), and phos-AKT1 (#bs-1448R, Bioss Biotech, Beijing, China) at 4°C overnight and with appropriate horseradish peroxidase (HRP)-conjugated secondary antibodies (1:10,000 dilution; Proteintech, Chicago, IL, USA) for 60 min at ambient temperature.

Techniques: In Vivo, Immunohistochemical staining, Staining, TUNEL Assay, Injection

Journal: BMC Cancer

Article Title: microRNA-451a promoter methylation regulated by DNMT3B expedites bladder cancer development via the EPHA2/PI3K/AKT axis

doi: 10.1186/s12885-020-07523-8

Figure Lengend Snippet: DNMT3B/miR-451a/EPHA2/PI3K/AKT axis modulates BCa cell growth in vivo. T24 cells (2 × 10 6 cells/mL) with stable poor expression of DNMT3B or miR-451a were injected into the right armpit of NOD/SCID mice. a , from the fifth day, the growth rate of T24 cells was evaluated by measuring the volume every 5 days in vivo; b , tumor weight; c , KI67 staining intensity in tumors evaluated by immunohistochemistry; d , EPHA2 staining intensity in tumors evaluated by immunohistochemistry; e , phos-PI3K staining intensity in tumors evaluated by immunohistochemistry; f , phos-AKT1 staining intensity in tumors evaluated by immunohistochemistry. Data are represented as the means ± SD from three independent assays. Statistically significant differences were calculated using one-way or two-way ANOVA, followed by Tukey’s multiple comparison test. ** p < 0.01 vs mice injected with cells transfected with sh-NC or sh-DNMT3B + inhibitor NC

Article Snippet: The antibodies used in the experiments were DNMT3B (#72335, Cell Signaling Technologies (CST), Beverly, MA, USA), phos-PI3K (#ab182651, Abcam, Cambridge, UK), phos-AKT1 (#44-621G, Thermo Fisher Scientific Inc., Waltham, MA, USA), EPHA2 (#37–4400, Thermo Fisher), KI67 (#9027, CST), glyceraldehyde-3-phosphate dehydrogenase (GAPDH, #ab181602, Abcam), horseradish peroxidase (HRP)-labeled goat anti-mouse (#G-21040, Thermo Fisher) or goat anti-rabbit IgG (#G-21234, Thermo Fisher).

Techniques: In Vivo, Expressing, Injection, Staining, Immunohistochemistry, Transfection