Objective: To investigate the differential expression of microRNA (miRNA) in patients with endometrial cancer and its relationship with prognosis and survival. Method: We used The Cancer Genome Atlas (TCGA) database to analyze differentially expressed miRNAs in endometrial cancer tissues and adjacent normal tissues. In addition, we successfully screened out key microRNAs to build nomogram models for predicting prognosis and we performed survival analysis on the key miRNAs as well. Result: We identified 187 differentially expressed miRNAs, which includes 134 up-regulated miRNAs and 53 down-regulated miRNAs. Further univariate Cox regression analysis screened out 47 significantly differentially expressed miRNAs and selected 12 miRNAs from which the prognostic nomogram model for ECA patients by LASSO analysis was constructed. Survival analysis showed that high expression of hsa-mir-138-2, hsa-mir-548f-1, hsa-mir-934, hsa-mir-940, and hsa-mir-4758 as well as low-expression of hsa-mir-146a, hsa-mir-3170, hsa-mir-3614, hsa-mir-3616, and hsa-mir-4687 are associated with poor prognosis in EC patients. However, significant correlations between the expressions levels of has-mir-876 and hsa-mir-1269a and patients’ prognosis are not found. Conclusion: Our study found that 12 significantly differentially expressed miRNAs might promote the proliferation, invasion, and metastasis of cancer cells by regulating the expression of upstream target genes, thereby affecting the prognosis of patients with endometrial cancer.
Autoimmune bullous diseases (AIBDs) are a group of chronic disorders characterized by blister formation resulting from abnormal immune responses. Janus kinase (JAK) inhibitors have emerged as promising therapeutic agents for AIBDs. This review discusses the use of JAK inhibitors—such as upadacitinib, baricitinib, tofacitinib, and abrocitinib, among others—in the management of various AIBDs. We examine clinical evidence supporting their efficacy in conditions including bullous pemphigoid, pemphigus foliaceus, mucous membrane pemphigoid, paraneoplastic pemphigus, and other blistering diseases. Additionally, the review covers histological findings related to JAK inhibition, the role of the JAK/STAT signaling pathway in AIBD pathogenesis and treatment, and the therapeutic benefits of different JAK inhibitors. Finally, we highlight the potential of these agents to improve clinical outcomes, while also acknowledging the limitations of existing research.