GSTA2 (Glutathione S-Transferase Alpha 2)

Mutant p53 downregulated the expression of GSTA2 and subsequently increased DNA damage. The combination of p53 mutation and dysregulated oxidative response likely promotes the genomic instability that initially drives the transformation to high grade serous ovarian carcinoma.

Further cost-effectiveness studies and ethnically diverse prediction models are needed to demonstrate the impact of pharmacogenomic testing on ACT prognosis and clinical decision-making prior to adoption. PROSPERO identifier CRD42024557946.

Furthermore, pathway analysis demonstrated that these hub genes were mainly linked to pathways involved in chemical carcinogenesis, metabolic processes, steroid hormone biosynthesis, retinol metabolism, linoleic acid metabolism, arachidonic acid metabolism, inflammatory mediator regulation, Ras, and protein processing in the endoplasmic reticulum. In conclusion, this study provides important insights into the molecular mechanisms underlying Cd-induced liver damage.

Accordingly, treatment with the antioxidant N-acetyl cysteine (NAC) partially rescued melanocyte expansion. Together, our data establish a critical function for BMI1 in McSC maintenance that reflects a partial role for suppression of oxidative stress, and likely transcriptional repression of Cdkn2a.

AA IC significantly increased the transcription of SOD1, GSTA2, and GSTP1 genes (p < 0.05), while AA IC significantly decreased mRNA for CYP2E1 in H4IIE cells (p < 0.05). Obtained results indicate that AA treatments, both in vivo and in vitro, change hepatocytes; drug-metabolizing potential and disturb its redox status.

Our findings identify novel molecular candidates that potentially drive and modify the disease differentially among these histotypes.

Moreover, isatin significantly reduced the DENA/2-AAF-induced decrease in hepatic expression of anti-apoptotic Bcl2 and the DENA/2-AAF-induced increases in pro-inflammatory and pro-apoptotic factors (TNF-α, NF-κB p50, NF-κB p65, p53, and caspase 3). Thus, it can be concluded that isatin may protect against chemically induced hepatocarcinogenesis by enhancing cellular antioxidant, anti-inflammatory, and detoxification mechanisms, in part through upregulation of the Nrf2 signaling pathway.