Long noncoding RNA (lncRNA) has been recognized as a regulator of gene expression, and the dysregulation of lncRNAs is involved in the progression of many types of cancer, including epithelial ovarian cancer (EOC). To explore the potential roles of lncRNAs in EOC, we performed lncRNA and mRNA microarray profiling in malignant EOC, benign ovarian cyst and healthy control tissues. In this study, 663 transcripts of lncRNAs were found to be differentially expressed in malignant EOC compared with benign and normal control tissues. We also selected 18 altered lncRNAs to confirm the validity of the microarray analysis using quantitative real-time PCR (qPCR). Pathway and Gene Ontology (GO) analyses demonstrated that these altered transcripts were involved in multiple biological processes, especially the cell cycle. Furthermore, Series Test of Cluster (STC) and lncRNA-mRNA co-expression network analyses were conducted to predict lncRNA expression trends and the potential target genes of lncRNAs. We also determined that two antisense lncRNAs (RP11-597D13.9 and ADAMTS9-AS1) were associated with their nearby coding genes (FAM198B, ADAMTS9), which participated in cancer progression. This study offers helpful information to understand the initiation and development mechanisms of EOC.

To evaluate the effects of maternal vitamin D deficiency on body fat and adipogenesis in offspring rats, and explore the potential mechanism, we constructed a vitamin D deficient rat model and performed metabolic activity evaluation, body fat monitoring, biochemical analysis, adipogenesis assay, methylation microarray and RNA-seq for their offspring rats. We found the weight of vitamin D deficient (VDD) offspring was gradually higher than that of control (CLT) offspring, and the difference was significant since 10 weeks old. When compared with CTL offspring, the 24 h heat production, peak blood glucose, adipose tissue volume and blood lipid indexes were significantly increased in VDD offspring at 14 weeks old. Moreover, a significant increase in proliferation rate and number of lipid droplets for pre-adipocytes was also observed in VDD offspring group. DNA methylation profiling showed that compared to CTL group, 608 promoters and 204 CpG islands were differentially methylated in the VDD group, involving 305 genes. When combined with the results of RNA-seq, 141 genes of the methylated genes were differentially expressed. In conclusion, vitamin D deficiency during pregnancy may promote the proliferation and differentiation of pre-adipocytes, which may be associated with methylation alterations of genes, ultimately leading to offspring obesity.

Lung cancer is the most aggressive tumour afflicting patients on a global scale. Extracellular vesicle (EV)‐delivered microRNAs (miRs) have been reported to play critical roles in cancer development. The current study aimed to investigate the role of hypoxic bone marrow mesenchymal cell (BMSC)‐derived EVs containing miR‐328‐3p in lung cancer. miR‐328‐3p expression was determined in a set of lung cancer tissues by RT‐qPCR. BMSCs were infected with lentivirus‐mediated miR‐328‐3p knock‐down and then cultured in normoxic or hypoxic conditions, followed by isolation of EVs. Following ectopic expression and depletion experiments in lung cancer cells, the biological functions of miR‐328‐3p were analysed using CCK‐8 assay, flow cytometry and Transwell assay. Xenograft in nude mice was performed to test the in vivo effects of miR‐328‐3p delivered by hypoxic BMSC‐derived EVs on tumour growth of lung cancer. Finally, the expression of circulating miR‐328‐3p was detected in the serum of lung cancer patients. miR‐328‐3p was highly expressed in EVs derived from hypoxic BMSCs. miR‐328‐3p was delivered to lung cancer cells by hypoxic BMSC‐derived EVs, thereby promoting lung cancer cell proliferation, invasion, migration and epithelial‐mesenchymal transition. miR‐328‐3p targeted NF2 to inactivate the Hippo pathway. Moreover, EV‐delivered miR‐328‐3p increased tumour growth in vivo. Additionally, circulating miR‐328‐3p was bioactive in the serum of lung cancer patients. Taken together, our results demonstrated that hypoxic BMSC‐derived EVs could deliver miR‐328‐3p to lung cancer cells and that miR‐328‐3p targets the NF2 gene, thereby inhibiting the Hippo pathway to ultimately promote the occurrence and progression of lung cancer.