Background: Early-onset preeclampsia (EOPE) is a serious pregnancy disorder with multisystem complications. Recently, circRNA was reported to participate in the progression of EOPE. However, the role and mechanism of circRNA_06354 in the pathophysiological development of EOPE remain unclear. Methods: Blood samples from patients with EOPE and healthy pregnant controls (CTRL) were analyzed by RNA-seq. functions and mechanisms of circRNA_06354 in EOPE were investigated by a series of experiments. An EOPE rat model was constructed to detect the expression levels of circRNA_06354. Results: The level of circRNA_06354 was altered in EOPE and CTRL individuals, as well as EOPE and CTRL rats. CircRNA_06354 had a sensitivity of 88.9% and a specificity of 100% in predicting EOPE. Subcellular localization indicated that circRNA_06354 was primarily detected in the cytoplasm of HTR8-/SV-neo cells and the cytotrophoblast of EOPE placentas. In addition, circRNA_06354 transcription was markedly higher than that of its linear counterpart. RNA pull-down assays implied that hsa-miR-92a-3p might sponge circRNA_06354. Vascular endothelial growth factor-A (VEGF-A) levels were found to be increased in EOPE patients. Moreover, overexpression of circRNA_06354 suppressed the migration, invasion and tube formation of trophoblastic cells invading spiral arteries or the endometrium. Conclusion: CircRNA_06354 inhibits trophoblastic cell invasion, migration and tube formation toward the endometrium in the initiation of EOPE. The circRNA_06354/hsa-miR-92a-3p/VEGF-A axis might be a therapeutic target in the prevention and treatment of EOPE.

Intrahepatic cholangiocarcinoma (ICC) is the second common primary hepatic malignancy tumor. In this study, an integrative analysis of differentially expressed genes (DEGs) and miRNAs from the ICC onset and adjacent normal tissues were performed to explore the regulatory roles of miRNA–mRNA interaction. A total of 1018 DEGs and 39 miRNAs were likely involved in ICC pathogenesis, suggesting the changes in cell metabolism in ICC development. The built network indicated that 30 DEGs were regulated by 16 differentially expressed miRNA. The screened DEGs and miRNA together were probably considered the biomarkers of ICC, and their important roles in ICC pathogenesis remain to be elucidated. This study could provide a good basis to uncover the regulatory mechanism of miRNA and mRNAs in ICC pathogenesis.