Long Non-coding RNA ADAMTS9-AS2 Suppresses Biological Functions of Ovarian Cancer Cells Through Recruiting DNMTl and Up-regulating SEPT6

Objective: The mechanism of long non-coding RNA ADAM metallopeptidase with thrombospondin type 1 motif, 9 antisense RNA 2 (ADAMTS9-AS2) has been insufficiently explored in ovarian cancer (OC). Here, the action of ADAMTS9-AS2 in OC with the involvement of DNA methyhransferase l (DNMT1) and septin 6 (SEPT6) was explored. Methods: Epithelial OC tissue and ovarian epithelial tissue specimens were collected to test ADAMTS9-AS2, DNMT1 and SEPT6 expression. An appropriate cell line was screened out and transfected with highly expressed ADAMTS9-AS2 or SEPT6 or lowly expressed DNMT1 to detect their roles in biological functions of OC cells. Tumorigenesis of OC cells in nude mice was projected to validate cell experiment results. The interactions between ADAMTS9-AS2 with DNMT1/SEPT6 were tested. Results: Elevated DNMT1 and reduced ADAMTS9-AS2 and SEPT6 were detected in OC. ADAMTS9-AS2 bound to both DNMT1 and SEPT6. Restoring ADAMTS9-AS2 or SEPT6 or depleting DNMT1 diminished OC cell viability, invasion and migration, arrested cell cycle and accelerated apoptosis in vitro, and repressed tumor growth in vivo. Conclusion: Collectively, ADAMTS9-AS2 fights against OC through recruiting DNMT1 and up-regulating SEPT6.