Western blot assay was performed to further confirm these results by analysis of cell cycle-related proteins (PCNA,
Cyclin A,
Cyclin E1, CDK2,
Cyclin D1, and CDK4).
Semiquantitative evaluation of labelings of
cyclins (B1, D1) and E-cadherin in untreated and vanadyl sulphate treated MCF-7 cells.
As shown in Figure 2, in the spleen, gene expression of
cyclin A2 (Group SP-3 d vs Group Con-3 d; Group SP-6 d vs Group Con-6 d; Group SP-9 d vs Group Con-9 d) significantly increased but p21 (Group SP-3 d relative to Group Con-3 d) and
cyclin D3 (Group SP-9 d relative to Group Con-9 d) markedly decreased (p<0.05), and no significant difference was found in
cyclin E2 mRNA abundance that was induced by spermine intake (p>0.05).
A significant cycle x time interaction existed for
cyclin D1 (p = 0.014, effect size, 0.756).
Effect of Extract on Bcl-2,
Cyclin B1 and Ki67 Expression
The main role of the synthetic complex
cyclin E/Cdk2 is to phosphorylate pRBp to pRBpp, followed by phosphorylation of p27 to degrade, and when p27 is degraded, the cells cross the G1/S test point and enter the S period.
The antibodies used in this study include FGF21 (1: 1000, Abcam, USA), MyoD (1: 500, Santa Cruz, USA), MyoG (1: 500, Santa Cruz, USA), MEF2c (1: 500, Santa Cruz, USA), MHC (1: 500, Santa Cruz, USA), CDK4 (1:1000, CST, USA), P21 (1:1000, R&D, USA), P53 (CST)
Cyclin D1 (1: 1000, R&D, USA),
Cyclin D3 (1: 1000, R&D, USA), and tubulin (1: 1000, Abcam, USA), which were diluted with 5% BSA.
growth hormones that directly target
Cyclin E/CDK2 complex which on activation hyper- phosphorylate the pRb at G1.
Conclusion: In conclusion, our findings strongly suggest that CA promotes a profound deregulation of cell cycle control and reduces the survival of GBM cells via proteasome-mediated degradation of
Cyclin Bl, RB and SOX2.
All these effects of thapsigargin on MH7A cells were mediated by the reduction of
cyclin D1 mRNA and protein levels, which were mediated by mTOR.
Expression levels of
cyclins (
cyclins A1, A2, B1, B2, D1, D2, and F), CDKs (CDK1 and CDK2), and E2Fs (E2F1 and E2F2) increase, whereas cell cycle inhibitors (Cdkn1a and Cdkn2a) decrease in islets of betatrophin-injected mice compared to control-injected mice.
In addition to the increased
cyclin D2 in the nucleus and the increased expression of active caspase 3, which were demonstrated in this work, we previously reported increased translocation of p53 to the nucleus, which is a signal that activates apoptotic death in mature neurons [18].
