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首页> 外文期刊>Biochemistry and Cell Biology >The lncRNA TUG1 promotes cell growth and migration in colorectal cancer via the TUG1-miR-145-5p-TRPC6 pathway
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The lncRNA TUG1 promotes cell growth and migration in colorectal cancer via the TUG1-miR-145-5p-TRPC6 pathway

机译:LNCRNA Tug1通过Tug1-MiR-145-5P-TRPC6途径促进细胞生长和迁移结直肠癌

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Colorectal cancer (CRC) is the third-most prevalent malignant tumor. Taurine upregulated gene 1 (TUG1), a long non-coding RNA ( lncRNA), is reportedly involved in the physiological and pathological processes of CRC. However, the role of TUG1 in the progression of CRC and its underlying mechanisms are largely unknown. Here, we measured the expression of TUG1 in clinical samples from CRC patients and found that the expression level of TUG1 was higher in CRC tissues compared with the normal adjacent tissues. We then performed knockdown of TUG1 with siRNAs in two CRC cell lines and found that TUG1 knockdown inhibited the viability, proliferation, and migration of CRC cells, and reduced the ability of CRC cells to form subcutaneous tumors. Furthermore, we discovered that TUG1 affects the cellular processes in CRC cells by sponging miR-145-5p. We further found that miR-145-5p inhibits the expression of the protein-encoding gene Transient Receptor Potential Cation Channel Subfamily C Member 6 (TRPC6), and that overexpression of TRPC6 restored the inhibitory role of miR145-5p in CRC cells. In conclusion, we have demonstrated that TUG1 exerts its role by modulating the TUG1-miR-145-5pTRPC6 regulatory axis, thus revealing a novel molecular mechanism for the effects of TUG1 in the progression of CRC. Our data indicate that the TUG1-miR-145-5p-TRPC6 signaling pathway could serve as a target for the diagnosis and treatment of CRC.
机译:结肠直肠癌(CRC)是第三次普遍的恶性肿瘤。据报道,牛磺酸上调基因1(Tug1),长期非编码RNA(LNCRNA),参与CRC的生理和病理过程。然而,Tug1在CRC进展中的作用以及其潜在机制的作用在很大程度上是未知的。在这里,我们测量了来自CRC患者的临床样本中Tug1的表达,发现与正常相邻的组织相比,CRC组织中Tug1的表达水平较高。然后,我们在两个CRC细胞系中与siRNA进行了敲击Tug1,发现Tug1敲低抑制CRC细胞的可行性,增殖和迁移,并降低了CRC细胞形成皮下肿瘤的能力。此外,我们发现Tug1通过冲水-145-5P影响CRC细胞中的细胞过程。我们进一步发现MiR-145-5P抑制蛋白质编码基因瞬时受体电位阳离子通道亚家族C成员6(TRPC6)的表达,并且TRPC6的过度表达恢复了CRC细胞中miR145-5p的抑制作用。总之,我们已经证明,Tug1通过调节Tug1-MiR-145-5PTRPC6调节轴来施加其作用,从而揭示了Tug1在CRC进展中的新的分子机制。我们的数据表明,Tug1-MiR-145-5P-TRPC6信号通路可以作为CRC诊断和治疗的目标。

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