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首页> 外文期刊>Journal of cellular biochemistry. >LncRNA PTCSC3/miR‐574‐5p Governs Cell Proliferation and Migration of Papillary Thyroid Carcinoma via Wnt/β‐Catenin Signaling
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LncRNA PTCSC3/miR‐574‐5p Governs Cell Proliferation and Migration of Papillary Thyroid Carcinoma via Wnt/β‐Catenin Signaling

机译:LNCRNA PTCSC3 / miR-574-5P通过Wnt /β-catenin信号传导治理乳头状甲状腺癌的细胞增殖和迁移

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摘要

ABSTRACT The distance metastases of papillary thyroid carcinoma (PTC) were a major threaten for PTC patients, thus, to study the potential mechanism for the treatment of PTC was essential. Previous studies have shown that PTCSC3 (Thyroid Carcinoma Susceptibility Candidate 3), miR‐574‐5p and Wnt/β‐catenin were involved in PTC, but the potential pathogenic mechanism among them was still unclear. Real‐time PCR and Western blot were used to detect genes expression. Luciferase reporter assay was used to detect the combination of miR‐574‐5p and suppressor of cancer cell invasion (SCAI), as well as the ratio of TOP/FOP. RNA Pull‐down assay verified the bound of PTCSC3 and miR‐574‐5p. MTT assay, Transwell assay, and wound scratch assay were used to detect cell viability and cell migration. The expression of PTCSC3 and SCAI were decreased, while miR‐574‐5p and β‐catenin were increased in PTC tissues and cells. Overexpressed PTCSC3 suppressed cell proliferation and migration, promoted the expression of SCAI, but inhibited β‐catenin. PTCSC3 absorbed miR‐574‐5p, and miR‐574‐5p targeted to SCAI; SCAI could regulate the activity of Wnt/β‐catenin. PTCSC3/miR‐574‐5p regulated the activity of Wnt/β‐catenin via SCAI and mediated cell proliferation and migration of PTC‐1. In vivo experiments verified the fact that overexpressed PTCSC3 inhibited tumor growth. The signaling PTCSC3‐miR‐574‐5p‐SCAI‐Wnt/β‐catenin mediated the proliferation and migration of PTC‐1 cells, which was vital for the further PTC therapy and prognosis. J. Cell. Biochem. 118: 4745–4752, 2017. ? 2017 Wiley Periodicals, Inc.
机译:摘要乳头状甲状腺癌(PTC)的距离转移是PTC患者的主要威胁,因此研究了PTC治疗的潜在机制至关重要。以前的研究表明,PTCSC3(甲状腺癌敏感性候选候选者3),miR-574-5p和wnt /β-catenin参与了PTC,但它们中的潜在致病机制仍不清楚。使用实时PCR和Western印迹来检测基因表达。荧光素酶报告器测定用于检测miR-574-5p和癌细胞侵袭(scai)的抑制剂的组合,以及顶/掺杂的比例。 RNA下拉测定验证了PTCSC3和MIR-574-5P的界限。 MTT测定,Transwell测定和伤口划痕测定用于检测细胞活力和细胞迁移。降低PTCSC3和SCAI的表达,而MIR-574-5P和β-Catenin在PTC组织和细胞中增加。过表达的PTCSC3抑制细胞增殖和迁移,促进了SCAI的表达,但抑制了β-catenin。 PTCSC3吸收MiR-574-5P,并针对SCAI的MIR-574-5P; SCAI可以调节Wnt /β-catenin的活性。 PTCSC3 / miR-574-5P通过SCAI和介导的细胞增殖和PTC-1的迁移调节WNT /β-Catenin的活性。体内实验证实了过表达PTCSC3抑制肿瘤生长的事实。信号PTCSC3-MIR-574-5P-SCAI-WNT /β-Catenin介导PTC-1细胞的增殖和迁移,这对于进一步的PTC治疗和预后至关重要。 J.Cell。生物学习。 118:4745-4752,2017。 2017年Wiley期刊,Inc。

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