MicroRNAs (miRNAs) have been demonstrated to regulate the progression of numerous types of cancer, including acute myeloid leukemia (AML). Previous studies demonstrated that miR-1271-5p functions as a tumor suppressor; however, the roles of miR-1271-5p in AML remain unknown. In the present study, miR-1271-5p was significantly downregulated in AML tissues compared with normal tissues by reverse transcription-quantitative polymerase chain reaction analysis. Furthermore, the expression levels of miR-1271-5p in patients with AML may function as a prognostic marker. In addition, overexpression of miR-1271-5p significantly suppressed the proliferation and induced apoptosis of AML cells by Cell Counting kit-8 and fluorescence activated cell sorter assays; miR-1271-5p downregulation exhibited opposing effects. Additionally, transcription factor ZIC2 may be a direct target of miR-1271-5p in AML cells, which was demonstrated by a luciferase reporter assay and RNA pulldown assay. Overexpression of miR-1271-5p significantly reduced the mRNA and protein expression levels of ZIC2 in AML193 and OCI-AML2 cells by reverse transcription-quantitative polymerase chain reaction analysis and western blotting. Furthermore, an inverse correlation between miR-1271-5p and ZIC2 expression in AML samples was observed. In summary, ZIC2 was upregulated in AML tissues, and restoration of ZIC2 expression was able to promote the proliferation and reduce the apoptosis of AML cells transfected with miR-1271-5p mimics. The results of the present study demonstrated that miR-1271-5p inhibited the progression of AML by targeting ZIC2.

Background: Osteosarcoma (OS) is a quite malignant bone cancer. However, how long noncoding RNA (lncRNA) regulates OS progression remains poorly investigated. The present study aims to illustrate the potential functions of lncRNA MYOSLID in the regulation of OS progression. Methods: The expression of YOSLID, miR-1286 and RAB13 was analyzed by qRT-PCR. Cell proliferation was determined via CCK8 and colony formation assays. Transwell assay was used to examine migration and invasion. The luciferase reporter assay, RNA pulldown and RNA immunoprecipitation (RIP) assays were utilized to detect the interactions among MYOSLID, miR-1286 and RAB13. Results: The expression of MYOSLID was upregulated in OS tissues and cell lines. MYOSLID overexpression predicted poor prognosis in OS patients. MYOSLID knockdown suppressed proliferation, migration and invasion of OS cells. MYOSLID was the sponge for miR-1286 and inhibited its expression while miR-1286 targeted RAB13 directly. MYOSLID promoted RAB13 expression via sponging miR-1286. Conclusion: Our work demonstrated that the MYOSLID/miR-1286/RAB13 axis is a novel regulatory signaling in promoting OS progression.

Introduction MiR-200c plays a central role in glucose metabolism in cancer cells. However, its upstream regulators in this process are unknown. CircRNA CSPP1 (circCSPP1) was predicted to bind to premature miR-200c, an oncogenic miRNA. Therefore, we explored their interaction in osteosarcoma (OS). Methods Differential circCSPP1 and miR-200c expression in OS was analyzed using RT-qPCR. Glucose metabolism was analyzed by glucose uptake assay. Subcellular circCSPP1 location in OS cells was detected using cellular fractionation assay. The direct interaction between circCSPP1 and miR-200c was explored using RNA-RNA pull-down assay. The role of circCSPP1 in miR-200c maturation was investigated by analyzing both mature and premature miR-200c levels in OS cells with circCSPP1 overexpression. Results CircCSPP1 and premature miR-200c levels were increased while mature miR-200c level was decreased in OS. CircCSPP1 was detected in both the nuclear and cytoplasm fractions of OS cells. CircCSPP1 directly interacted with premature miR-200c. CircCSPP1 overexpression increased premature miR-200c level, glucose uptake, and cell proliferation, but decreased mature miR-200c level. MiR-200c overexpression suppressed the role of circCSPP1 in OS cells. Conclusions CircCSPP1 promotes OS cell proliferation and increases glucose metabolism by suppressing miR-200c maturation.