Yuan Xie

A case report of endometrial stromal sarcoma with sex-cord differentiation

IGF2BP3 Knockdown Induces Ferroptosis by Inhibiting Autophagy‐Mediated EMC2 Degradation in Ovarian Cancer

ABSTRACT Recent studies have increasingly demonstrated that chemoresistance in ovarian cancer primarily stems from resistance to oxidative stress and ferroptosis. Ferroptosis, a non‐apoptotic form of cell death dependent on intracellular iron and marked by the buildup of lipid reactive oxygen species (ROS), has shown enhanced effectiveness in triggering cell death in ovarian cancer cells. Thus, this study aimed to explore the potential of gene knockdown associated with ferroptosis as an innovative therapeutic strategy against ovarian cancer. Up‐regulated genes were identified using a gene bank, and their expression levels were validated through Western blotting (WB) and quantitative PCR (qPCR). Levels of MDA, Fe 2+ , GSH, ROS, SQSTM1, LC3‐I and LC3‐II in ovarian cancer cells treated with sorafenib and subjected to gene knockout were assessed using specific kits. Expression levels of proteins related to ferroptosis were analyzed by WB. Tumor size, volume, ferroptosis and autophagy in ovarian cancer tumor tissues were also examined. IGF2BP3 was elevated in human ovarian cancer and decreased during ferroptosis induced by sorafenib in human ovarian cancer cells. IGF2BP3 knockdown inhibited ovarian cancer cell function and promoted ferroptosis, in addition to autophagy‐mediated EMC2 degradation. IGF2BP3 knockdown increased ovarian cancer sensitivity to sorafenib. This study confirmed that IGF2BP3 knockdown inhibited ovarian cancer cell malignancy, promoted ferroptosis and inhibited autophagy‐mediated EMC2 degradation, and verified that IGF2BP3 knockdown increased the sensitivity to sorafenib in ovarian cancer mice.

Identification of prognostic biomarkers for endometrioid endometrial carcinoma based on the miRNA and mRNA co‐expression network regulated by estradiol

Endometrioid Endometrial Carcinoma (EEC), an estradiol-related disease, remains a serious health threat to women because of its high incidence and trend of rejuvenation. Accumulating evidence has highlighted that microRNAs (miRNAs) and messenger RNAs (mRNAs) play important roles in various biological processes involved in the pathogenesis of EEC. This study aimed to identify the potential prognostic biomarkers associated with EEC regulated by estradiol. RNA expression profiles of EEC were obtained from The Cancer Genome Atlas database (n = 408) and the original sequencing, which was performed on endometrial cancer Ishikawa cells treated with 250 nM estradiol (n = 3), 50 nM estradiol (n = 3) or control (n = 3). The TargetScan database was used to predict the target genes of prognosis-related differentially expressed miRNAs (DEMs). Subsequently, functional enrichment analysis and topological analysis were performed on the overlaps of target genes and differentially expressed mRNAs (DEGs). Kaplan-Meier analysis was used to predict prognosis-related target genes to identify prognostic biomarkers and cell population landscapes, and gene expression analysis was performed to locate prognosis-related DEGs based on single-cell transcriptomic sequencing data from the NCBI Sequence Read Archive database. Four estradiol-related DEGs were associated with prognosis, and 235 overlapping target DEGs were screened and incorporated into the functional enrichment analysis and protein-protein interaction network visualization studies. Additionally, SACS and GPR157 were identified as potential biomarkers for EEC prognosis through survival analyses. Furthermore, single-cell transcriptome data were analyzed to show changes in gene expression levels in specific cell types. This study demonstrates that miR-142-5p-SACS and miR-30a-5p-GPR157, which are regulated by estradiol, may hold promise as diagnostic and prognostic biomarkers and novel therapeutic targets for EEC.