CASP3 overexpression

Casp3 + cells were also significantly more sensitive to cisplatin than mock cells with Ic50 of 158.4 μM and 219.5uM respectively according to MTT assay which confirmed by apoptosis assay. Hence, targeting Caspase-3 as a therapeutic approach may enhance the cancer cell sensitivity to chemotherapy, but also increase the cancer cell proliferation, metastases and invasion which may works as a double edge sword. understanding the effects of Caspase 3 over expression on cancer cells could inspire innovative therapies targeting its non-apoptotic actions, potentially improving cancer treatment outcomes.

GA-CDs demonstrated potent anticancer properties by inducing apoptosis and reducing cell viability in HCT-116 cells. These findings suggest the potential of GA-CDs as a novel therapeutic agent for colorectal cancer treatment, warranting further investigation into their mechanism of action and in vivo efficacy.

Octahydroquinazoline 10 displayed an increase in caspase-3 by 1.12 folds compared to standard colchicine and induce apoptosis and demonstrated cell cycle arrest in G2/M phase arrest by targeting p53 pathway. Analogue 10 has considerably promoted cytotoxic radiation activity and boosted apoptotic induction in HepG-2 cells by 1.5 fold higher than standard colchicine.

The treated groups (except 6) had significantly higher expression of Bax/Caspase 3 genes and lower expression of Bcl-2 genes than the control group (P < 0.05, 0.01). Coadministration of Dox with probiotics and vitamin D3 showed promising results in reducing tumor size, protecting intestinal tissue and influencing gene expression, suggesting a strategy to enhance the effectiveness of breast cancer treatment while reducing side effects.

In vitro analyses revealed significant anti-cancer effects of SPGE extract in MCF-7 and MDA-MB-231 cell lines (cytotoxicity, caspase-3/-7, Bcl-2, Annexin V/PI, cell cycle, BrdU, and mitochondrial membrane potential). Our study demonstrates the significant chemopreventive and treatment effects of salvia haulm using animal or in vitro BC models.

The more excellent ratios of infiltrating CD8+/CD4+ T cells, the decreased invasion of regulatory FOXP3+ Treg lymphocytes, and the increased apoptosis brought on by Caspase9/Caspase-3 overexpression and Survivin downregulation may all contribute to the consequences. Our findings suggest that in people with advanced GC, H. pylori pIRES2-DsRed-Express-ureF DNA vaccines may have immunotherapeutic utility.

The findings of this research illustrated the suppression of BATF3 as an effective targeted therapy strategy for CML.

Overexpression of caspase-3 and GSDME accelerated irradiation-induced ICD. In summary, irradiation in EC cells induces GSDME-mediated pyroptosis and activates ICD to inhibit esophageal carcinoma cell survival.

Cellular assays revealed a synergistic effect of sinensetin on IFNγ -triggered anticancer action in HepG2 cells through overexpression of caspase-3 mRNA and protein. In conclusion, this study may hold great promise for the development of potential ligand- protein complexes for therapeutic purposes.

What is more, CASP3 overexpression or CD274 knockdown promoted the role of ononin in TC cells. Ononin treatment induced the cell death of the TC cells through regulating the CASP3 and CD274 expressions.

In addition, ipconazole at 50 µM induced an overexpression of Bax, Casp3, APAF1, and BNIP3 (cell death genes); NLRP3, Casp1, and IL1B (inflammasome complex genes); and NFκB, TNFα, and IL6 (inflammation genes); it also reduced the expression of NRF2, SOD, and GPx (antioxidant genes). Our results show that ipconazole produces cytotoxic effects by reducing cell viability, generating oxidative stress, and inducing cell death in SH-SY5Y cells, so ipconazole exposure should be considered as a factor in the presentation of neurotoxicity or neurodegeneration.