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首页> 外文期刊>Nucleosides, nucleotides and nucleic acids >Has_circ_0048764 promotes breast cancer progression by sponging miR-578 and regulating HMGA2 expression
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Has_circ_0048764 promotes breast cancer progression by sponging miR-578 and regulating HMGA2 expression

机译:Has_circ_0048764 通过海绵化 miR-578 和调节 HMGA2 表达来促进乳腺癌进展

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BackgroundCircular RNAs (circRNAs) function as important regulators in the progression of cancers. The role of circRNA_0048764 (circ_0048764) in the development of breast cancer (BC) remains inconclusive. This work investigates the biological function and molecular mechanism of circ_0048764 in BC.MethodsQuantitative real-time PCR (qRT-PCR) was conducted to measure the expression levels of circ_0048764, microRNA-578 (miR-578) and high mobility group AT-hook 2 (HMGA2) mRNA. The viability of BC cells was examined by cell counting kit 8 (CCK-8) assay. Besides, cyclin D1, proliferating cell nuclear antigen (PCNA) and HMGA2 expression levels were detected by western blot. The migrative and invasive capability of BC cells were probed by transwell assay. The relationships between miR-578 and circ_0048764 or HMGA2 3 '-UTR were validated by dual-luciferase reporter gene assay.ResultsCirc_0048764 was highly expressed in BC tissues and cells, which was significantly associated with tumor size (>= 2 cm), lymph node status (positive), and higher TNM stage of BC patients. Circ_0048764 depletion suppressed the proliferative, migrative, and invasive abilities of BC cells, which was rescued by transfection of miR-578 inhibitors. The binding sites were verified between circ_0048764 and miR-578. HMGA2 was identified to be a target of miR-578 in BC cells, and circ_0048764 positively regulated HMGA2 expression in BC cells via repressing miR-578.ConclusionCirc_0048764 promotes BC cell growth, migration and invasion via absorbing miR-578 and up-regulating HMGA2.
机译:背景环状RNA(circRNA)在癌症进展中起着重要的调节因子作用。circRNA_0048764(circ_0048764)在乳腺癌(BC)发展中的作用仍不确定。本研究探讨了BC中circ_0048764的生物学功能和分子机制。方法采用实时荧光定量PCR(qRT-PCR)检测circ_0048764、microRNA-578(miR-578)和高迁移率组AT-hook 2(HMGA2)mRNA的表达水平。通过细胞计数试剂盒 8 (CCK-8) 测定法检测 BC 细胞的活力。此外,Western blot检测细胞周期蛋白D1、增殖细胞核抗原(PCNA)和HMGA2表达水平。通过transwell法检测BC细胞的迁移和侵袭能力。miR-578与circ_0048764或HMGA2 3'-UTR的关系通过双荧光素酶报告基因检测进行验证。ResultsCirc_0048764在BC组织和细胞中高表达,与BC患者的肿瘤大小(>=2 cm)、淋巴结状态(阳性)和较高的TNM分期显著相关。Circ_0048764耗竭抑制了 BC 细胞的增殖、迁移和侵袭能力,这可以通过转染 miR-578 抑制剂来挽救。在 circ_0048764 和 miR-578 之间验证了结合位点。HMGA2 被鉴定为 BC 细胞中 miR-578 的靶标,并通过抑制 miR-578 circ_0048764正调控 BC 细胞中 HMGA2 的表达。ConclusionCirc_0048764通过吸收 miR-578 和上调 HMGA2 促进 BC 细胞的生长、迁移和侵袭。

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