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Long noncoding RNA small nucleolar RNA host gene 12 promotes papillary thyroid carcinoma cell growth and invasion by targeting miR16-5p

机译:长的非致RNA小核仁RNA宿主基因12通过靶向mir16-5p来促进乳头状甲状腺癌细胞生长和侵袭

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摘要

Emerging evidence has shown that long noncoding RNA (lncRNA) plays an important role in various types of malignant cancer. Small nucleolar RNA host gene 12 (SNHG12) was found to be upregulated and to act as an oncogene in several cancers. However, the function and regulatory mechanism of SNHG12 remain unclear in papillary thyroid carcinoma (PTC). In this study, SNHG12 was found to be increased in PTC tissues and cell lines using quantitative real-time PCR. Knockdown of SNHG12 significantly inhibited PTC cell proliferation, migration and invasion and induced apoptosis in vitro. Mechanistic investigations revealed that SNHG12 functions as a competing endogenous RNA (ceRNA) to sponge miR-16-5p, which was downregulated in PTC tissues. In addition, rescue assays further confirmed that SNHG12 contributed to the progression of PTC through regulating miR-16-5p expression. These results indicated that SNHG12 might contribute to tumor progression in PTC by acting as a ceRNA to sponge miR-16-5p.
机译:新兴的证据表明,长期非致rna(lncrna)在各种类型的恶性癌症中起重要作用。 发现小核仁RNA宿主基因12(SNHG12)被上调并用作几种癌症中的癌基因。 然而,SNHG12的功能和调节机制在乳头状甲状腺癌(PTC)中仍不清楚。 在本研究中,发现SNHG12在PTC组织和细胞系中使用定量实时PCR增加。 SNHG12的敲低显着抑制PTC细胞增殖,迁移和侵袭和体外诱导的细胞凋亡。 机械研究表明,SNHG12用作竞争的内源性RNA(Cerna),以海绵MiR-16-5P,其在PTC组织中下调。 此外,进一步证实SNHG12通过调节miR-16-5P表达有助于PTC的进展。 这些结果表明,通过作为CERNA来强化MIR-16-5P,SNHG12可能有助于PTC中的肿瘤进展。

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