failure is highly generated. 4 Massive efforts are needed to improve the therapy of AMI.MicroRNAs (miRNAs) are a class of endogenic, non-coding single-stranded RNAs, approximately 21-25 nucleotides long. 5 MiRNAs participate in many biological processes such as cell growth, proliferation, apoptosis and differentiation, and many miRNAs have been reported to be indicated in various oncological and cardiovascular diseases. 6 Recent studies have shown that miR-1 and miR-208, which are the heart-specific or heart-enriched miRNAs, can be released into circulating blood after AMI. 7 The miR-208 family includes miR-208a, miR-208b and miR-499. MiR-208a is encoded by the intron of the

Malignant melanoma (MM) is an invasive tumor that poses a threat to patient health. Circular RNAs (circRNAs) are important regulators of MM carcinogenesis. In this study, we investigated the expression characteristics and biological functions of, and mechanism underlying, circ_0119872 expression in MM. METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was employed to examine the circ_0119872, microRNA (miR)-582-3p, and E2F transcription factor 3 (E2F3) mRNA expression levels in MM tissues and cell lines. Western blotting was performed to quantify E2F3 protein expression. MM cells with circ_0119872 knockdown were established, and cell counting kit 8 (CCK-8) and transwell assays were utilized to examine the function of circ_0119872 and its effects on the malignant characteristics of MM cells. The MiRDB and TargetScan databases were used to predict the target genes of miR-582-3p. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was used to explore the biological functions of the target genes of miR-582-3p. Additionally, a dual-luciferase reporter gene experiment was performed to verify the targeting relationship between circ_0119872 and miR-582-3p as well as that between miR-582-3p and E2F3. RESULTS: Circ_0119872 was remarkably upregulated in MM tissues and cell lines. Circ_0119872 knockdown suppressed the cell proliferation and metastasis In addition, miR-582-3p was identified as a downstream target of circ_0119872. The target genes of miR-193a-3p are involved in melanogenesis and cancer-related signaling pathways. Mechanistically, circ_0119872 facilitated MM progression by adsorbing miR-582-3p and upregulating E2F3 expression. CONCLUSION: Circ_0119872 is an oncogenic circRNA that participates in the promotion of MM progression by regulating the miR-582-3p/E2F3 axis.

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Gastric cancer is one of the most common types of malignant tumor of the gastrointestinal tract worldwide. Cisplatin (DDP) is a commonly used chemotherapeutic drug in the clinic; however, the resistance of gastric cancer cells to DDP limits its efficacy. In the present study, drug-resistant gastric cancer cell lines were constructed using the stepwise continuous selection method, and the relative expression levels of long non-coding RNA (lncRNA) CDKN2B antisense RNA 1 (ANRIL) and microRNA (miR)-181a-5p were detected using reverse transcription-quantitative PCR. The knockdown of lncRNA ANRIL and miR-181a-5p expression was performed by transfection with shRNA-ANRIL and an miR-181a-5p inhibitor, respectively. Cellular proliferation and sensitivity to DDP were assessed using Cell Counting Kit-8 analysis. Cell apoptosis and cell cycle distribution were assessed using flow cytometry and western blotting. The binding relationships between ANRIL, miR-181a-5p and cyclin G1 (CCNG1) were verified using a dual luciferase reporter assay. The results revealed that the expression levels of miR-181a-5p were downregulated in all drug-resistant cell lines. ANRIL-knockdown inhibited cellular proliferation, and promoted apoptosis and cell cycle arrest; however, following the knockdown of miR-181a-5p, the inhibition of cell cycle arrest was alleviated. Notably, miR-181a-5p, ANRIL and CCNG1 were found to have targeting relationships. In conclusion, the findings of the present study suggested that knocking down the expression of ANRIL inhibited cellular proliferation, and promoted apoptosis and cell cycle arrest. Furthermore, its downstream target, miR-181a-5p, inhibited the proliferation of drug-resistant cells and enhanced their sensitivity to DDP.

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