Fig 1: HMGA1 regulates cyclin E2 and Cdk2 expressions in MDA-MB-231 cells. Western blot analyses assess cyclinE2 and Cdk2 protein expression in MDA–MB–231 cells silenced for HMGA1 (siA1_3) or treated with control siRNA (siCTRL). Representative WB analyses, on the left, are shown together with red ponceau stained membrane to verify total protein normalization. The histogram graph on the right refers to densitometric analysis of western blot (siCTRL and siA1_3). Bars indicate the mean. Standard deviations are shown (n = 3). Statistical significance was assessed with Student’s t-test (*: p ≤ 0.05; ***: p ≤ 0.001).
Fig 2: miR-672-3p and DNAJC2 influences the activation of the p-AKT pathways in CRC cells. (A) Expression of AKT, p-AKT and P21 was evaluated by western blotting in DLD-1 and HCT-116 cell lines compared with NC after the transfection of siRNA or plasmid. (B) Expression of Cyclin D1, CDK2, AKT, p-AKT and P21 was evaluated by western blotting in DLD-1 and HCT-116 cell lines after treating with miR-672-3p mimics or inhibitor. miR/miRNA, microRNA; DNAJC2, DnaJ Heat Shock Protein Family (Hsp40) Member C2; CRC, colorectal cancer; p-, phosphorylated; NC, negative control; si, small interfering.
Fig 3: Knockdown of PTEN or WWOX attenuated the effects of miR-214 inhibitor on cell-cycle- and apoptosis-associated proteins and AKT signaling pathway in 5–8F cell line. (A) Expression levels of WWOX, PTEN, AKT signaling-associated proteins in 5–8F cells. (B) Levels of cell-cycle-associated proteins CDK2/6, p27, and cyclin D1 in 5–8F cells after indicated treatment. (C) Levels of cell-apoptosis-associated proteins in 5–8F cells after indicated treatment. ***p < 0.001 and **p < 0.01.
Fig 4: The key genes related to cell cycle and EMT process were regulated by SP1/RNASEH2A. A. Overexpression of SP1 strengthened the level of CDK1 and CDK2, whereas the addition of si-RNASEH2A diminished the effect of SP1-OE. B. Upregulation of SP1 increased the level of N-cadherin, Snail1, Snail2, Vimentin, and decreased E-cadherin, whereas the administration of si-RNASEH2A inhibited the effect of SP1-OE on N-cadherin, Snail1, Snail2, Vimentin and E-cadherin expression. **p < 0.01 vs. si-con, ##p < 0.01 vs. si-RNASEH2A, &&p < 0.01 vs. SP1-OE.
Fig 5: Depletion of RNASEH2A significantly blocked the cell cycle, invasion and migration in HepG2 and Hep3B cells. A. In HepG2 and Hep3B cells, si-RNASEH2A-1 or si-RNASEH2A-2 stimulation obviously decreased the protein levels of CDK1 and CDK2. B. In HepG2 and Hep3B cells, si-RNASEH2A-1 or si-RNASEH2A-2 stimulation obviously reduced the number of cell invaded. C. In HepG2 and Hep3B cells, si-RNASEH2A-1 or si-RNASEH2A-2 stimulation obviously reduced the cell migration distance. **p < 0.01 vs. si-con. Scale bar = 50 μm.
Supplier Page from Abcam for Anti-Cdk2 antibody