In this study we analyzed the involvement of DLGAP1-AS2 in OC, and explored the in vitro interaction between DLGAP1-AS2 and miR-16. We found that DLGAP1-AS2 was significantly overexpressed in OC and it may suppress the maturation of miR-16 to promote cell invasion and migration.
In a recent study Miao et al reported that DLGAP1-AS2 was significantly overexpressed in glioma and its downregulation suppressed the metastasis and growth of tumors but induced cancer cell apoptosis . In addition, the authors found that the functions of DLGAP1-AS2 in glioma are likely mediated by the upregulation of YAP1 . Based on our knowledge, the expression pattern and function of DLGAP1-AS2 in other cancers is unknown. In this study we found that DLGAP1-AS2 was significantly overexpressed in OC, and overexpression of DLGAP1-AS2 increased the invasion and migration of OC cells. Therefore, DLGAP1-AS2 may play oncogenic roles in OC by promoting tumor metastasis.
MiR-16 has been characterized as a tumor suppressor miRNA in different types of cancers, including OC [13, 15]. In OC, miR-16 is downregulated in OC and its overexpression suppresses Wnt/β‑catenin signaling pathway to decrease the invasion and migration of cancer cells . Consistently, our study confirmed the downregulation of both mature miR-16 and miR-16 precursor in OC, and the inhibitory effects of miR-16 overexpression on OC cell invasion and migration.
Previous studies of miR-16 mainly focused on the downstream targets of miR-16 in cancer biology [13, 15]. However, the upstream regulators of miR-16, such as the factors regulating the biogenesis, such as the maturation, of miR-16 have not been well studied. In this study we showed that overexpression of DLGAP1-AS2 could suppressed the maturation of miR-16 in OC cells. Although the in vivo interaction between DLGAP1-AS2 and miR-16 is unknown, we observed the inverse correlation between DLGAP1-AS2 and mature miR-16, but not between DLGAP1-AS2 and miR-16 precursor across OC tissues. Therefore, DLGAP1-AS2 may also suppress the maturation of miR-16 in OC patients. However, the mechanism remains elusive. In a recent study Yu et al. showed that lncRNA CCAT2 may suppress the movement of miR-145 precursor from nucleus to cytoplasm, thereby suppressing the maturation of miR-145. Therefore, we speculate that DLGAP1-AS2 may also suppress the transportation of miR-16 in OC cells. However, studies are needed to test our speculation.
In conclusion, DLGAP1-AS2 is overexpressed in OC and it may suppress the maturation of miR-16 to promote OC cell invasion and migration.