Xiaoning Wei

Prevalence characteristics of cervical human papillomavirus genotypes in Nanning, China: A 10‐year survey of 77,756 women from one medical center

AbstractObjectivesThe prevalence of human papillomavirus (HPV) infection and HPV genotypes varies in different regions. However, there is little data on HPV prevalence and genotyping in Guangxi Province, South China. This study conducted a 10‐year survey in a health center, to estimate the prevalence characteristics of HPV genotypes.MethodsBy using polymerase chain reaction (PCR) amplification and nucleic acid molecular hybridization, the HPV genotypes were detected from 77,756 females who were patients of the Department of Obstetrics and Gynecology and those who visited the Health Management Center for a physical examination between August 2011 and November 2020. The prevalence, genotypes, age‐related HPV infections, as well as chronological change of HPV prevalence, and the HPV genotype distribution were analyzed.ResultsThe overall prevalence of HPV infection was 21.14% (16,439/77,756). The HPV infection rate differed significantly between the patients of the Department of Obstetrics and Gynecology and the women who underwent a physical examination (22.98% vs. 9.88%, p < 0.05). The prevalence rates of high‐risk HPV, low‐risk HPV, mixed HPV (mixed high‐risk, and low‐risk HPV infection), and multiple HPV infections were 18.96% (14,739/77,756), 4.09% (3178/77,756), 1.90% (1478/77,756), and 4.94% (3838/77,756), respectively. The most prevalent genotypes were HPV 52, 16, and 58. The age‐associated HPV prevalence showed bimodal curves, with the first peak at <25 years and the second peak at >56 years.ConclusionsThis study provides baseline data on the HPV prevalence in the general female population of Nanning, Guangxi Province. Women <25 and >56 years old faced the greatest threat of HPV infection, and HPV 52, 16, and 58 were the most common genotypes.

Erastin induces ferroptosis in cervical cancer cells via Nrf2/HO-1 signaling pathway

Objective Our research aims to assess the influence of erastin, a ferroptosis-inducing agent, on cervical cancer cells. Introduction Cervical cancer is a prevalent malignancy in females. Dysregulation of ferroptosis, a form of cell demise reliant on iron, is implicated in several cancers. Methods The effect of erastin on HeLa and SiHa was detected by transwell assay, scratch test, and colony formation assay, while cell apoptosis was detected using flow cytometry. Cellular reactive oxygen species (ROS) generation was detected using the dichloro-dihydro-fluorescein diacetate assay. Sequencing analysis identified differentially expressed genes (DEGs), and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) Enrichment analyses were employed to identify the target gene. Subsequently, the utilization of small interfering RNA (siRNA) was employed to suppress the targeted gene expression in HeLa cells, thereby effectively mitigating the impact of erastin on various cellular processes including invasion, colony formation, migration, and ROS generation. Results The findings indicate that erastin attenuates the viability of both HeLa cells (IC50 = 30.88 µM) and SiHa cells (IC50 = 29.40 µM). Treatment with erastin at 10 µM inhibits the invasion, colony formation, and migration of both HeLa and SiHa cells within 24 h. Ferrostatin-1 (1 µM) notably alleviates the inhibitory effects of erastin of HeLa and SiHa cells. Upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream target, heme oxygenase-1 (HO-1), was found in erastin-treated cells compared to the control group. When knocked down HO-1 in HeLa cells, effectively counteracting the effects of erastin on the invasion, colony formation, migration, and ROS production in HeLa cells. Conclusion Our research demonstrates that erastin induces ferroptosis and the accumulation of ROS in cervical cancer cells by activating the Nrf2/HO-1 pathway, significantly reducing cell proliferation and motility. These findings propose a potential molecular mechanism of erastin-mediated cervical cancer development.