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Long intergenic noncoding RNA 00707 promotes colorectal cancer cell proliferation and metastasis by sponging miR-206

机译:长的基因间非编码RNA 00707通过使miR-206变海绵促进大肠癌细胞的增殖和转移

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Background: The incidence and mortality of colorectal cancer (CRC) are rising worldwide. Long-noncoding RNAs (lncRNAs) are known to play key roles in the development of human cancers, including CRC. However, the function and underlying mechanism of long intergenic noncoding RNA 00707 (LINC00707) in the development of CRC are unknown. Materials and methods: The expression of LINC00707 and miR-206 in tissue samples or cell lines was measured by quantitative reverse transcription PCR (qRT-PCR). The protein expression of neurogenic locus notch homolog protein 3 (NOTCH3) and transmembrane 4 L6 family member 1 (TM4SF1) was assessed by Western blotting. Cell proliferation, migration, and invasion were assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and transwell assays. Luciferase reporter assay and biotin-coupled miRNA capture assay were used to explore the relationship between LINC00707 and miR-206 expression. Results: The expression of LINC00707 was significantly upregulated in CRC tissues as compared with the adjacent non-CRC tissues. LINC00707 expression was significantly correlated with tumor size, lymphatic metastasis, and distant metastasis, but not significantly correlated with age and gender. Knockdown of LINC00707 expression significantly inhibited LoVo and HCT116 cell proliferation, migration, and invasion. LINC00707 acted as a molecular sponge by competing for miR-206 and indirectly modulating the expression of its targets, NOTCH3 and TM4SF1. Conclusion: LINC00707 promotes CRC cell proliferation and metastasis by sponging miR-206, suggestive of its potential application for CRC treatment.
机译:背景:全球大肠癌(CRC)的发病率和死亡率正在上升。众所周知,长非编码RNA(lncRNA)在包括CRC在内的人类癌症的发展中起着关键作用。但是,长的基因间非编码RNA 00707(LINC00707)在CRC发生中的功能和潜在机制尚不清楚。材料和方法:通过定量逆转录PCR(qRT-PCR)测量LINC00707和miR-206在组织样品或细胞系中的表达。通过蛋白质印迹法评估神经源性基因座缺口同源蛋白3(NOTCH3)和跨膜4 L6家族成员1(TM4SF1)的蛋白表达。细胞增殖,迁移和侵袭通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物(MTT)和transwell分析进行评估。使用荧光素酶报告基因测定法和生物素偶联的miRNA捕获测定法来探讨LINC00707与miR-206表达之间的关系。结果:与邻近的非CRC组织相比,LINC00707的表达在CRC组织中显着上调。 LINC00707表达与肿瘤大小,淋巴转移和远处转移显着相关,但与年龄和性别无显着相关。敲低LINC00707表达可显着抑制LoVo和HCT116细胞的增殖,迁移和侵袭。 LINC00707通过竞争miR-206并间接调节其靶标NOTCH3和TM4SF1的表达来充当分子海绵。结论:LINC00707通过刺激miR-206促进CRC细胞的增殖和转移,提示其在CRC治疗中的潜在应用。

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