Retraction of "XRCC1 and hOGG1 polymorphisms and endometrial carcinoma: A meta-analysis".

[This retracts the article DOI: 10.1515/med-2024-0913.].

XRCC1 and hOGG1 polymorphisms and endometrial carcinoma: A meta-analysis.

Endometrial carcinoma's (EC) etiology is complex and involves DNA repair gene polymorphisms like XRCC1-Arg399Gln and hOGG1-Ser326Cys, but their association with the disease is unclear. Following PRISMA, we conducted a systematic review and meta-analysis, collecting data from four databases. The studies needed to be population-based case-control studies examining the association between the named polymorphisms and EC. Quality was assessed with the Newcastle-Ottawa Scale. Pooled odds ratios (OR) and 95% confidence intervals (CI) were calculated, and subgroup analyses were conducted based on ethnicity. Seven studies were included. Both polymorphisms were found to significantly increase EC risk, particularly in Caucasians. XRCC1-Arg399Gln showed a dominant model OR of 1.14 (95% CI: 1.01-1.29) and a homozygous model OR of 1.59 (95% CI: 1.12-2.25). The heterozygote model OR for hOGG1-Ser326Cys was 1.29 (95% CI: 1.02-1.63), and the allele OR was 1.31 (95% CI: 1.07-1.60). XRCC1-Arg399Gln and hOGG1-Ser326Cys may increase EC risk, primarily in Caucasian women, emphasizing the role of DNA repair in disease susceptibility. More extensive studies are needed to validate these findings in diverse ethnicities and investigate other DNA repair gene polymorphisms.

Inhibiting LCN2 can suppress the development of NSCLC by promoting ferroptosis.

BACKGROUND: Tumor progression is intricately linked to ferroptosis, a recently discovered form of regulated cell death. However, the specific causes of ferroptosis in non-small cell lung cancer (NSCLC) remain unclear. METHODS: In this study, we conducted transcriptome sequencing on NSCLC samples and identified Lipocalin-2 (LCN2) as a significantly differentially expressed gene associated with ferroptosis in NSCLC. Through the intersection of the set of significantly different genes with ferroptosis-related genes, we unveiled the relevance of LCN2 in NSCLC. To validate our findings, several cell lines (BEAS-2B, A549, H1299, PC-9, H1975) were utilized, and Western blot (WB) analysis was performed. We employed a variety of assays, including CCK8, EDU, scratch, Transwell, and specific assays targeting ferroptosis, to investigate the effects of LCN2 on NSCLC cell proliferation, migration, and ferroptosis. Additionally, LCN2 was evaluated in vivo using a mouse tumor xenograft model. RESULTS: In both NSCLC patients and cells, LCN2 exhibited upregulation and was associated with a poor prognosis. Inhibition of LCN2 promoted ferroptosis, resulting in the inhibition of NSCLC proliferation and migration. Conversely, the ferroptosis inhibitor Fer-1 promoted NSCLC cell proliferation and migration while inhibiting ferroptosis. Furthermore, down-regulating LCN2 reduced Fer-1's promotion of NSCLC cell migration and proliferation, as well as its prevention of ferroptosis. In vivo inhibition of LCN2 prevented NSCLC cell growth and enhanced ferroptosis. CONCLUSION: Based on our research, reducing LCN2 could effectively induce ferroptosis and hinder the growth of NSCLC.

Relationship between positive margin and residual/recurrence after excision of cervical intraepithelial neoplasia: a systematic review and meta-analysis.

Background: The relationship between endocervical and ectocervical margin status and residual or recurrence after cervical intraepithelial neoplasia (CIN) resection has been controversial. We investigated the relationship between the excision margins and residual/recurrence to assess indicators for the scope of resection and the risk of treatment failure by using meta-analysis. Methods: Literature searches were performed in PubMed, Medline, Embase, Central, Wangfang and CNKI databases. Patients after CIN resection were grouped according to whether there was residual or recurrence, and the differences in exposure factors between the two groups were compared. Or they were grouped by exposure factor, and compare the differences in residual and recurrence rates under different grouping conditions. The observed outcome was postoperative residual or recurrence. The risk of bias in the literature was assessed using the Newcastle-Ottawa Scale (NOS). The chi-square test were used for heterogeneity. Subgroup explored the sources of heterogeneity. Publication bias was assessed using funnel plots and Egger's test. Results: A total of 11 studies were included in this study, 8 studies were at low risk of bias and 3 studies were at high risk of bias. The 11 studies included 3065 patients, 774 patients with positive margins and 2,291 patients with negative margins. The rate of residual/recurrence after excision of CIN in patients with positive margins was significantly higher than in patients with negative margins [odds ratio (OR) =3.99, P<0.00001]. There was no heterogeneity among the studies (P=0.16), with publication bias (P<0.05). The residual/recurrence rate was significantly higher in patients with positive endocervical margins than in patients with negative endocervical margins (OR =2.59, P<0.00001). There was no heterogeneity among studies (P=0.78) and no publication bias (P<0.05). There was no significant difference in residual/recurrence rate between positive and negative ectocervical margins (OR =1.14, P=0.36). There was no heterogeneity among studies (P=0.32) and no publication bias (P<0.05). Conclusions: Positive endocervical margins, but not external cervical margins, are risk factors for residual/recurrence of CIN after resection. Close attention to the status of the endocervical margins is recommended. More aggressive treatment and frequent follow-up are needed for patients with positive endocervical margins.

RNF168 suppresses the cancer stem cell-like traits of nonsmall cell lung cancer cells by mediating RhoC ubiquitination.

The critical roles of E3 ubiquitin ligase RNF168 have been widely revealed in various tumors, however, its roles in lung cancer progression are still confusing. Here, we found that RNF168 expression is positively correlated with the overall survival, first-progression survival, and postprogression survival of lung adenocarcinoma, but not correlated with these survivals of squamous cell carcinoma of lung. Furthermore, it was shown that RNF168 mRNA expression is lowly expressed in lung adenocarcinoma tissues, but highly expressed in squamous cell carcinoma of lung. Functional experiments indicated that RNF168 overexpression significantly suppressed the cancer stem cell (CSC)-like traits of nonsmall cell lung cancer (NSCLC) cells, as characterized by the attenuation of sphere-formation ability, ALDH activity, and the expression of lung CSC markers. Mechanistic studies demonstrated that RNF168 facilitated the ubiquitination of RhoC, which had been considered as a fascinating target for CSCs, and thus promoted RhoC protein degradation. Notably, RNF168 failed to affect the mRNA expression of RhoC and overexpression of RhoC rescued the inhibitory effects of RNF168 overexpression on the CSC-like traits of NSCLC cells. Therefore, this study revealed RNF168 as a novel regulator of RhoC protein in NSCLC cells, this RNF168/RhoC regulatory axis might be a potential target for NSCLC treatment.

Covalent Immobilization of Cellulase onto Amino and Graphene Oxide Functionalized Magnetic Fe2O3/Fe3O4@SiO2 Nanocomposites.

Magnetic Fe2O3/Fe3O4@SiO2 nanocomposites were prepared via the citric-alcohol solution combustion process. The obtained nanocomposites were characterized with SEM, XRD, VSM, TEM, EDS, HRTEM, and FTIR techniques. The results revealed that the magnetic Fe2O3/Fe3O4@SiO2 nanocomposites were successfully obtained with the average grain size of 87 nm and the saturation magnetization of 36 emu/g. After the surface of magnetic Fe2O3/Fe3O4@SiO2 nanocomposites was functionalized by amino group, the amino-functionalized Fe2O3/Fe3O4@SiO2-NH2 nanocomposites were loaded onto graphene oxide based on Mitsunobu reaction. Subsequently, the cellulase was immobilized onto Fe2O3/Fe3O4@SiO2-NH-GO nanocomposites by a glutaraldehyde-mediated Schiff base reaction. The immobilization conditions were optimized by adjusting the pH, temperature, and cellulase dose. The results revealed that optimized immobilization conditions were determined to be temperature of 50 °C, pH of 5, and cellulase solution of 0.1 mL. 97.3% cellulase were successfully immobilized under the optimal conditions. The catalytic performances of the immobilized cellulase were also evaluated. The maximum activity was achieved at pH 4, and 50 °C with cellulase solution of 0.4 mL.