Background:　Many　microRNAs　(miRs)　are　dysregulated　in　cancers,　and　aberrant　miR　expression　patterns　have　been　suggested　to　correlate　with　chemo-resistance　of　cancer　cells.　We　aim　to　study　the　role　of　miR-30　family　members　in　cisplatin-resistance　of　ovarian　cancer　cells.　Methods:　qRT-PCR　was　used　to　compare　differential　expression　levels　of　miR-30　family　members　in　ovarian　cancer　cell　line　A2780　and　its　cisplatin-resistant　derivative　CP70.　Changes　of　cisplatin-sensitivity　in　miR-30a-5p-　and　miR-30c-5p-overexpressed-CP70　cells　and　miR-30a-5p-　and　miR-30c-5p-inhibited-A2780　cells　were　examined　by　CCK8　assay　and　apoptosis　analysis　using　flow　cytometry;　targets　of　miR-30a/c-5p　were　analyzed　by　western　blotting　and　luciferase　reporter　assay;　methylation　regulation　of　pre-miR-30a/c-5p　was　examined　by　methylation　specific　PCR.　Results:　miR-30a-5p　and　miR-30c-5p,　in　contrast　to　other　miR-30　family　members,　dramatically　decreased　in　cisplatin-resistant　CP70　cells　due　to　overexpressed-DNMT1　induced　aberrant　methylation.　miR-30a/c-5p　in　turn　directly　inhibited　DNMT1　as　well　as　Snail.　Forced　expression　of　miR-30a/c-5p　or　knocking　down　of　DNMT1　and　Snail　promoted　cisplatin　susceptibility　and　partially　reversed　epithelial-mesenchymal　transition　(EMT)　in　CP70　cells,　while　inhibition　of　miR-30a/c-5p　or　ectopic　expression　of　DNMT1　and　Snail　induced　cisplatin　resistance　and　partial　EMT　in　cisplatin-sensitive　A2780　cells.　Conclusions:　A　feedback　loop　between　miR-30a/c-5p　and　DNMT1　is　a　potent　signature　for　cisplatin-resistance　and　EMT　in　ovarian　cancer,　promising　a　potential　target　for　improved　anti-cancer　treatment.　(C)　2017　The　Author(s)