ABSTRACT
OBJECTIVE: To explore whether rs4784227 polymorphism of CASC16 is correlated with risk of breast cancer. METHODS: Relevant studies up to December 24, 2020 were searched in PubMed, Embase, Web of Science, CNKI, VIP, and WANFANG databases. Data were analyzed by using Stata 12.0. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated, and country-based subgroup analyses were conducted. Sensitivity analysis was conducted to assess the stability of the results. Publication bias was assessed by using the Egger regression asymmetry test and visualization of funnel plots. RESULTS: Seven case-control studies enrolling 4055 breast cancer cases and 4229 controls were included. rs4784227 was found significantly associated with increased risk of breast cancer in a dominant (ORâ=â1.301, 95% CIâ=â1.190-1.423, Pâ<â.001), a recessive (ORâ=â1.431, 95% CIâ=â1.216-1.685, Pâ<â.001), and an allele model (ORâ=â1.257, 95% CIâ=â1.172-1.348, Pâ<â.001), while an over-dominant model showed that rs4784227 was correlated with decreased breast cancer risk (ORâ=â0.852, 95% CIâ=â0.778-0.933, Pâ=â.001). CONCLUSION: The rs4784227 polymorphism of CASC16 gene is correlated with breast cancer susceptibility.
Subject(s)
Apoptosis Regulatory Proteins/genetics , Breast Neoplasms/genetics , Trans-Activators/genetics , Alleles , Asian People , Case-Control Studies , Female , Genetic Predisposition to Disease , Humans , Odds Ratio , Polymorphism, Single Nucleotide , Risk FactorsABSTRACT
Nano-SiO2 is increasingly used in diagnostic and biomedical research because of its ease of production and relatively low cost and which is generally regarded as safe and has been approved for use as a food or animal feed ingredient. Although recent literature reveals that nano-SiO2 may present toxicity and DNA damage, however, the underlying mechanism remains poorly understood. Since in previous studies, we found that nano-SiO2 treatment down-regulated the expression of the poly(ADP-ribose) polymerases-1 (PARP-1), a pivotal DNA repair gene, in human HaCaT cells and PAPR-1 knockdown can aggravate DNA damage induced by nano-SiO2. Therefore, we speculate whether PARP-1 overexpression can protect DNA from damage induced by nano-SiO2. However, our data demonstrated that overexpression of PARP-1 in HaCaT cells slightly enhanced the cellular proliferation of undamaged cells, when compared with both empty vector control cells and parental cells, but had drastic consequences for cells treated with nano-SiO2. The PARP-1 overtransfected cells were sensitized to the cytotoxic effects and DNA damage of nano-SiO2 compared with control parental cells. Meanwhile, flow cytometric analysis of nano-SiO2 stimulated poly(ADP-ribose) synthesis revealed consistently larger fractions of cells positive for this polymer in the PARP-1 overexpression cells than in control clones. Combining our previous research on PARP-1 knockdown HaCaT cells, we hypothesize that an optimal level of cellular poly(ADP-ribose) accumulation exists for the cellular recovery from DNA damage.
