Preeclampsia (PE) is an idiopathic disease that occurs during pregnancy. It comprises multiple organ and system damage, and can seriously threaten the safety of the mother and infant throughout the perinatal period. As the pathogenesis of PE is unclear, there are few specific remedies. Currently, the only way to eliminate the clinical symptoms is to terminate the pregnancy. Although noncoding RNA (ncRNA) was once thought to be the “junk” of gene transcription, it is now known to be widely involved in pathological and physiological processes, including pregnancy-related disorders. Moreover, there is growing evidence that the unbalanced expression of specific ncRNA is involved in the pathogenesis of PE. In the present review, we summarize the expression patterns of ncRNAs, i.e., microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), and the functional mechanisms by which they affect the development of PE, and examine the clinical significance of ncRNAs as biomarkers for the diagnosis of PE. We also discuss the contributions made by genetic polymorphisms and epigenetic ncRNA regulation to PE. In the present review, we wish to explore and reinforce the clinical value of ncRNAs as noninvasive biomarkers of PE.

Osteosarcoma (OS) is the most common primary malignant bone tumor in children and adolescents with a high metastatic potential. Despite dramatic changes in OS treatments over the past decades, their efficiency is still limited and with severe complications and adverse side effects. Key mechanisms underlining tumorigenesis, metastasis and chemotherapy resistance are currently lacking, in turn hindering progress on developing effective and safe therapeutic strategies against OS. Recently, ADAMTS7, a member of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family, was shown to be involved in osteogenic differentiation related pathological processes. ADAMTS7 promotes vascular calcification via disturbing the balance between osteogenic BMP2 (regulating osteogenic differentiation and bone formation during development) and its natural inhibitor cartilage oligomeric matrix protein (Comp). Hence in this study, we aimed to investigate the role of ADAMTS7 in the pathological process of osteosarcoma. We first found ADAMTS7 was decreased in OS tissues. Lower expression of ADAMTS7 was correlated with poor histological differentiation and advanced clinical stage of OS. Through loss‐ and gain‐function analysis, we further revealed that ADAMTS7 attenuated cell proliferation, migration and invasion, while promoting the expression of osteogenic differentiation markers in two OS cell lines, MG63 and SAOS2. Moreover, Comp was responsible for the effects of ADAMTS7 on OS pathogenesis through reinforcing cell osteogenic differentiation mediated by BMP2 in vitro . In conclusion, ADAMTS7‐mediated degradation of Comp may provide a potential therapeutic target for the treatment of OS.