Abstract

ObjectivesMiR-140 and DNAJC3-AS1 have been demonstrated to play critical roles in cancer biology, while their participation in acute myeloid leukemia (AML) is unclear. This study aimed to explore the role of miR-140 and DNAJC3-AS1 in AML.MethodsThe expression of DNAJC3-AS1 and miR-140 were detected by RT-qPCR. Then, the role of DNAJC3-AS1 and miR-140 in regulating each other was explored by overexpression assay. Next, the direct interaction between DNAJC3-AS1 and miR-140 was analyzed using an RNA pull-down assay. Next, the subcellular location of DNAJC3-AS1 was explored using cellular, subcellular fractionation assay. Finally, cell proliferation analysis was evaluated with BrdU assay.ResultsIncreased expression levels of DNAJC3-AS1 and decreased expression levels of miR-140 were observed in AML patients. DNAJC3-AS1 was detected in nuclear and cytoplasm samples and direct interaction between DNAJC3-AS1 and miR-140 was observed.DiscussionReduced expression levels of DNAJC3-AS1 were observed after overexpression of miR-140 in AML cells. DNAJC3-AS1 increased cell proliferation and inhibited the role of miR-140 in suppressing cell proliferation.ConclusionIn conclusion, miR-140 may target DNAJC3-AS1 to suppress cell proliferation in AML.

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