Rescue experiments confirmed that the inhibition of miR-124 could reverse the effect of NEAT1 on RB cell proliferation, cycle arrest, apoptosis, and caspase-3 and -9 activities.
The apoptosis rate of RB cells declined (p < 0.001) when AEG-1 was overexpressed, in association with an upregulation of Bcl-2 protein and a downregulation of Bax protein and cleaved caspase-3 proteins.
Moreover, following siRNA HMGB1, siRNA NC and ammonium PDTC treatment, the apoptosis of RB cells with VCR incubation was evaluated by Hoechst staining, and the expression of cleaved caspase-3, cleaved poly(ADP-ribose) polymerase (PARP), Beclin 1 and p62 were determined with western blot analysis.
Reduction of RbAp48 led to the reduced suppression of proliferation and apoptosis induced by ALA‑PDT in cervical cancer cells, which was associated with a reduction in tumor suppressor protein 53 (p53), retinoblastoma (Rb), apoptosis‑related enzyme caspase‑3, and increased levels of the oncogenic genes, human papillomavirus E6 and E7.
Lentiviral vector-mediated overexpression of PAX6 in human retinoblastoma cells was associated with increased cell proliferation parallel to a reduced caspase-3-dependent apoptotic rate and a change in the p53 regulated cell cycle.
The tumor suppressor functions of miR-34a in RB cell lines were determined by tetrazolium-based cell growth assay and by caspase-3/7 and activated caspase-3 apoptotic activity assays.
This RbAp48-mediated transformation of HPV16 is probably because of the regulation by RbAp48 of tumor suppressors retinoblastoma and p53, apoptosis-related enzymes caspase-3 and caspase-8, and oncogenic genes, including E6, E7, cyclin D1 (CCND1), and c-MYC.
At 12 months of age, the APPswe/PS1-A246E/hCOX-2 triple-transgenic mice showed an elevation in the number of phosphorylated retinoblastoma (pRb) tumor suppressor protein and active caspase-3 immunopositive neurons, compared to double APPswe/PS1-A246E or single hCOX-2 transgenic controls.