Aim: To investigate exosomal RNAs (long noncoding RNAs (lncRNAs), microRNAs (miRNAs) and messenger RNAs (mRNAs)) profiling and their related networks in endometriosis (EMs). Materials & methods: RN...

Novel biomarkers are needed to accelerate the diagnosis and treatment of endometriosis. We performed RNA sequencing to explore the expression profiles of exosomal circular RNAs (circRNAs), microRNAs (miRNAs) and mRNAs in patients with ovarian endometriomas, eutopic endometria and normal endometria. Differentially expressed genes between the different pairs of groups were analyzed and functionally annotated. Then, miRNA-target RNA pairs were identified, competing endogenous RNA (ceRNA) scores were calculated, gene expression characteristics were determined, and these parameters were used to construct an exosomal ceRNA network. We identified 36 candidate hub genes with high degrees of gene connectivity. We also topologically analyzed the ceRNA network to obtain a hub ceRNA network of circRNAs with the highest closeness and ceRNA efficiency. Twelve genes overlapped between the 36 candidate hub genes and the genes in the hub ceRNA network. These 12 genes were considered to be exosomal RNA-based biomarkers, and circ_0026129/miRNA-15a-5p/ATPase H+ transporting V1 subunit A (ATP6V1A) were at the center of the ceRNA network. By determining the exosomal RNA expression profiles of endometriosis patients and constructing a circRNA-associated ceRNA network, these findings provide insight into the molecular pathways of endometriosis and new resources for its diagnosis and treatment.

Background: The modification of N6‐methyladenosine (m6A) plays a pivotal role in tumor by altering both innate and adaptive immune systems through various pathways, including the regulation of messenger RNA. The YTH domain protein family, acting as “readers” of m6A modifications, affects RNA splicing, stability, and immunogenicity, thereby playing essential roles in immune regulation and antitumor immunity. Despite their significance, the impact of the YTH domain protein family on tumor initiation and progression, as well as their involvement in tumor immune regulation and therapy, remains underexplored and lacks comprehensive review.Conclusion: This review introduces the molecular characteristics of the YTH domain protein family and their physiological and pathological roles in biological behavior, emphasizing their mechanisms in regulating immune responses and antitumor immunity. Additionally, the review discusses the roles of the YTH domain protein family in immune‐related diseases and tumor resistance, highlighting that abnormal expression or dysfunction of YTH proteins is closely linked to tumor resistance.Key points: This review provides an in‐depth understanding of the YTH domain protein family in immune regulation and antitumor immunity, suggesting new strategies and directions for immunotherapy of related diseases. These insights not only deepen our comprehension of m6A modifications and YTH protein functions but also pave the way for future research and clinical applications.

Aberrant upregulation and oncogenic roles of UBE2T are revealed in several cancers. However, the expression, clinical significance, and functions of UBE2T have not been explored in ovarian cancer (OC). In this study, the expression of UBE2T and its relation with clinicopathological features and prognosis of OC patients were explored by analyzing online data and experimental data. Besides, the functions of UBE2T in OC cells were investigated by in vitro experiments, including CCK-8, plate clone formation, and Transwell assays. Finally, the underlying mechanism of UBE2T associated functions in OC was analyzed. The results indicated that UBE2T was significantly upregulated in OC tissues. UBE2T expression was notably correlated with clinical features, such as primary T stage and FIGO stage in OC patients. UBE2T, acting as an independent prognostic indicator, was inversely associated with the prognosis of OC patients. The UBE2T knockdown remarkably suppressed the growth, proliferation, and invasion of OC cells, indicated by impaired cell viability, fewer cell clones, and invasive cells. Mechanistically, UBE2T depletion suppressed epithelial–mesenchymal transition (EMT), which was caused by autophagy activation due to inactivation of AKT/mTOR in OC cells with UBE2T knockdown. Collectively, our findings confirm that UBE2T upregulation predicts poor prognosis and promotes malignant progression in OC. UBE2T upregulation suppresses autophagy and subsequently boosts EMT via activating the AKT/mTOR axis, which accounts for the underlying mechanism of oncogenic roles of UBE2T in OC.

Background: Endometriosis is a common gynecological disorder with high rates of infertility and pelvic pain. However, its pathogenesis and diagnostic biomarkers remain unclear. This study aimed to elucidate potential hub genes and key pathways associated with endometriosis in ectopic endometrium (EC) and eutopic endometrium (EU).