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首页> 外文期刊>Cancer Cell International >LncRNA TTN-AS1 promotes the progression of oral squamous cell carcinoma via miR-411-3p/NFAT5 axis
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LncRNA TTN-AS1 promotes the progression of oral squamous cell carcinoma via miR-411-3p/NFAT5 axis

机译:LNCRNA TTN-AS1通过MIR-411-3P / NFAT5轴促进口腔鳞状细胞癌的进展

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Oral squamous cell carcinoma (OSCC) is a common kind of squamous cell carcinoma of the head and neck, which is a threat to public health. Long noncoding RNAs (lncRNAs) are associated with the development of various diseases, including cancers. LncRNA titin antisense RNA 1 (TTN-AS1) is known as a crucial regulatory factor in several cancers. Nevertheless, the specific functions of TTN-AS1 in OSCC remains obscure. The expression of TTN-AS1 in OSCC samples or cells was analyzed through qRT-PCR. Colony formation assay, EdU assay, flow cytometry assay, TUNEL assay and wound healing assay were conducted to estimate the functions of TTN-AS1 in OSCC cells. RIP and luciferase reporter assays were utilized to detect the interaction between TTN-AS1 and miR-411-3p as well as between miR-411-3p and NFAT5. TTN-AS1 expression was stronger in OSCC cells. Knockdown of TTN-AS1 effectively restrained cell proliferation and migration but had inductive role in apoptosis. Moreover, TTN-AS1 could function as the miR-411-3p sponge in OSCC and miR-411-3p exerted the inhibitory functions on OSCC cell growth. In addition, NFAT5 was proven as the target of miR-411-3p. Rescue assay indicated that overexpressing NFAT5 could reverse the inhibitory function of TTN-AS1 depletion on cell growth. lncRNA TTN-AS1 contributed to the progression of OSCC via miR-411-3p/NFAT5 axis.
机译:口腔鳞状细胞癌(OSCC)是头部和颈部鳞状细胞癌,这是对公共卫生的威胁。长度非编码RNA(LNCRNA)与各种疾病的发展有关,包括癌症。 LNCRNA三肽反义RNA 1(TTN-AS1)被称为几种癌症中的重要调节因子。然而,OSCC中TTN-AS1的特定功能仍然模糊。通过QRT-PCR分析OSCC样品或细胞中TTN-AS1的表达。进行菌落形成测定,进行EDU测定,流式细胞术测定,调节调节和伤口愈合测定以估计TTN-AS1在OSCC细胞中的功能。利用RIP和荧光素酶报告结果检测TTN-AS1和MIR-411-3P以及MIR-411-3P和NFAT5之间的相互作用。 OSCC细胞中TTN-AS1表达更强烈。 TTN-AS1的敲低有效抑制细胞增殖和迁移,但在凋亡中具有归纳作用。此外,TTN-AS1可以用作OSCC中的miR-411-3p海绵,MiR-411-3p施加对OSCC细胞生长的抑制功能。此外,NFAT5被证明是MIR-411-3P的目标。抢救测定表明,过表达NFAT5可以逆转TTN-AS1耗竭对细胞生长的抑制作用。 LNCRNA TTN-AS1通过MIR-411-3P / NFAT5轴促进OSCC的进展。

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