Retraction notice to "Potential of ß-elemene induced ferroptosis through Pole2-mediated p53 and PI3K/AKT signaling in lung cancer cells" [Chem. Biol. Interact. 365 (25 September 2022) 110088].

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Potential of ß-elemene induced ferroptosis through Pole2-mediated p53 and PI3K/AKT signaling in lung cancer cells.

Ferroptosis is crucial for tumor growth inhibition. Moreover, ferroptosis has been considered as a potential strategy against cancer. The present study focused on the mechanism of ferroptosis induction by ß-elemene during the lung cancer (extracted from the Chinese medicine Curcuma Wen yujin). CCK-8 assay, flow cytometry and biochemical assays including intracellular ROS, MDA, GSH, iron and 8-OHdG level were performed. DNA polymerase epsilon subunit 2 (Pole2) and the ferroptosis-related proteins were studied by utilizing western blotting. The study results showed that the ß-elemene reduced the viability of lung cancer cells via ferroptosis. Furthermore, multiple experiments confirmed that Pole2 knockdown enhanced the production of lipid ROS, MDA and iron, leading to the iron-dependent ferroptosis in lung cancer cells. Overexpression of Pole2 inhibited ß-elemene-induced ferroptosis through reduction of iron-dependent oxidative damage. Mechanically, Pole2 reduced the upregulation of p53 expression, and increased the phosphorylation levels of PI3K and AKT in ß-elemene-induced cells. Overexpression of TP53 or the inhibitor of PI3K/AKT pathway reversed the effects of Pole2. Together, ß-elemene evoked ferroptosis through the Pole2-regulated p53 or PI3K/AKT signalling, and might be an effective therapy for lung carcinogenesis.

Associations of FOXP3 gene polymorphisms with susceptibility and severity of preeclampsia: A meta-analysis.

OBJECTIVE: FOXP3 single nucleotide polymorphisms (SNPs) were recently elucidated to influence the development of preeclampsia (PE), but the results on this issue still remained controversial. Thus, a meta-analysis was implemented to systematically investigate the roles of FOXP3 SNPs in PE. METHODS: Eligible publications were identified by retrieving relevant electronic databases. Meanwhile, the association intensity was estimated by calculating odds ratios (ORs) and 95% confidence intervals (CIs) in various genetic models. RESULTS: Totally eight investigations involving 3446 subjects were enrolled in the final meta-analysis. The AC and AC + CC genotypes of FOXP3 rs3761548 were related to the susceptibility of PE in over-dominant (OR = 1.19, 95%CI = 1.02-1.38, P = 0.03) and recessive (OR = 0.59, 95% CI: 0.36-0.97, P = 0.04) models. Furthermore, correlation between rs2232365 and PE was observed in recessive model (GG vs. GA + AA) (OR = 0.79, 95%CI: 0.65-0.97, P = 0.03). Moreover, rs2232365 GA and GG + GA genotypes were associated with the severity of PE. However, rs4824747, rs3761547 and rs2280883 polymorphisms had no significant impact on PE susceptibility. CONCLUSIONS: FOXP3 rs3761548 and rs2232365 SNPs influenced the PE susceptibility and therefore may be potential biomarkers for prediction of PE risk.

Associations of methylenetetrahydrofolate reductase gene (MTHFR) rs1801131 and rs1801133 polymorphisms with susceptibility to vitiligo: A meta-analysis.

BACKGROUND: Vitiligo is a common pigmentary skin disorder, and genetic factors were acknowledged to be greatly associated with the pathogenesis of this disease. Recently, increasing studies investigated the associations of methylenetetrahydrofolate reductase (MTHFR) rs1801131 and rs1801133 polymorphisms with risks of vitiligo, but the results still remained controversial. AIM: The current meta-analysis was conducted to further evaluate the association of MTHFR polymorphisms with risk of vitiligo. METHODS: Eligible studies were searched in PubMed, EMBASE, Cochrane library, Chinese National Knowledge Infrastructure (CNKI), Technology of Chongqing (VIP), and Wan Fang Database until October 2020. All analyses were carried out using the Review Manager 5.3 software. RESULTS: A total of 6 studies that involved MTHFR rs1801131 and/or rs1801133 polymorphism were finally included, which enrolled 3599 participants. Our results showed that no correlations were found between MTHFR rs1801131, rs1801133 polymorphisms and vitiligo risks in overall group. However, subgroup analysis revealed that rs1801131 polymorphism was significantly associated with increased vitiligo risk in the allelic (C vs A: OR = 1.15, 95% CI = 1.02-1.29, P = .02) and homozygous models (CC vs AA: OR = 1.48, 95% CI = 1.10-2.01, P = .01) in Asian population and that the rs1801133 polymorphism was significantly associated with decreased vitiligo risk in the allelic model (T vs C: OR = 0.82, 95% CI = 0.74-0.92, P = .0005) also in Asian population. CONCLUSIONS: This meta-analysis confirmed the associations of MTHFR rs1801131 and rs1801133 polymorphisms with vitiligo risks and provided comprehensive insight into the pathogenesis of vitiligo.

Relationship between PPARα mRNA expression and mitochondrial respiratory function and ultrastructure of the skeletal muscle of patients with COPD.

Peripheral muscle dysfunction is an important complication in patients with chronic obstructive pulmonary disease (COPD). The objective of this study was to explore the relationship between the levels of peroxisome proliferator-activated receptor α (PPARα) mRNA expression and the respiratory function and ultrastructure of mitochondria in the vastus lateralis of patients with COPD. Vastus lateralis biopsies were performed on 14 patients with COPD and 6 control subjects with normal lung function. PPARα mRNA levels in the muscle tissue were detected by real-time PCR. A Clark oxygen electrode was used to assess mitochondrial respiratory function. Mitochondrial number, fractional area in skeletal muscle cross-sections, and Z-line width were observed via transmission electron microscopy. The PPARα mRNA expression was significantly lower in COPD patients with low body mass index (BMIL) than in both COPD patients with normal body mass index (BMIN) and controls. Mitochondrial respiratory function (assessed by respiratory control ratio) was impaired in COPD patients, particularly in BMIL. Compared with that in the control group, mitochondrial number and fractional area were lower in the BMIL group, but were maintained in the BMIN group. Further, the Z-line became narrow in the BMIL group. PPARα mRNA expression was positively related to mitochondrial respiratory function and volume density. In COPD patients with BMIN, mitochondria volume density was maintained, while respiratory function decreased, whereas both volume density and respiratory function decreased in COPD patients with BMIL. PPARα mRNA expression levels are associated with decreased mitochondrial respiratory function and volume density, which may contribute to muscle dysfunction in COPD patients.