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首页> 外文期刊>FEBS Open Bio >MicroRNA‐125a inhibits tumorigenesis by targeting Smurf1 in colorectal carcinoma
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MicroRNA‐125a inhibits tumorigenesis by targeting Smurf1 in colorectal carcinoma

机译：MicroRNA 125a通过靶向Smurf1抑制大肠癌的肿瘤发生

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摘要

Aberrant expression of microRNAs (miRNAs) may contribute to the initiation and development of multiple types of human cancer. Several miRNAs have been found to be strongly correlated with the diagnosis, progression, and prognosis of colorectal carcinoma (CRC), but the role of miR‐125a in CRC remains unclear. In the present study, the function of miR‐125a on the expression of Smad ubiquitin regulatory factor 1 (Smurf1) was investigated in?vitro and in?vivo . We verified that Smurf1 is a downstream target gene of miR‐125a and is involved in miR‐125a‐mediated regulation of CT26 cell (colon cancer cell) proliferation and migration. Overexpression of miR‐125a suppresses CT26 cell growth by inhibiting cell proliferation. Additionally, wound healing assays were performed to show that overexpression of miR‐125a significantly reduced CT26 cell migration, which was reversed by overexpression of Smurf1. In?vivo , miR‐125a overexpression downregulated the expression of Ki67 and Smurf1, thus leading to a marked reduction in tumor growth. These results revealed that miR‐125a plays a critical role in CRC by directly targeting Smurf1, a finding that may facilitate the development of improved diagnostic and therapeutic techniques for CRC.
机译：microRNA（miRNA）的异常表达可能有助于多种人类癌症的发生和发展。已发现几种miRNA与大肠癌（CRC）的诊断，进展和预后密切相关，但miR-125a在CRC中的作用仍不清楚。在本研究中，在体外和体内研究了miR-125a对Smad泛素调节因子1（Smurf1）表达的功能。我们证实Smurf1是miR-125a的下游目标基因，并参与miR-125a介导的CT26细胞（结肠癌细胞）增殖和迁移的调控。 miR-125a的过表达通过抑制细胞增殖来抑制CT26细胞的生长。此外，进行了伤口愈合试验，结果表明miR-125a的过表达显着降低了CT26细胞的迁移，而Smurf1的过表达可以逆转这种迁移。在体内，miR-125a过表达下调了Ki67和Smurf1的表达，从而导致肿瘤生长明显减少。这些结果表明，miR-125a通过直接靶向Smurf1在CRC中起着关键作用，这一发现可能有助于开发改进的CRC诊断和治疗技术。

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