背景:新的证据表明FAT10是肿瘤发生和发展的重要调节因子。FAT10在结直肠癌(CRC)中的特定作用的分子机制尚不清楚。
目的:为了研究FAT10是否参与增殖,CRC的侵袭和转移。
方法:本研究探讨了FAT10蛋白表达在CRC中的作用及临床意义。此外,FAT10的过表达和敲低实验旨在探讨其对CRC细胞迁移和增殖的影响。此外,探讨了FAT10调节钙蛋白酶小亚基1(Capn4)的分子机制。
结果:在这项研究中,与相应的正常组织相比,CRC组织中FAT10表达水平升高。此外,FAT10表达水平升高与晚期临床分期和CRC预后不良显著相关.此外,在CRC细胞中观察到FAT10的高表达,和FAT10的过表达显著增强了体内增殖,入侵,和细胞的转移,而FAT10的敲低在体内和体外环境中都抑制了所有这些细胞因子。此外,这项研究的结果表明,FAT10通过增强Capn4的表达来促进结直肠癌的进展,导致各种人类肿瘤的进展,正如以前的研究报告。FAT10促进CRC细胞增殖的机制,入侵,转移涉及Capn4的泛素化和降解过程的修饰。
结论:FAT10是CRC肿瘤发生和发展的重要调节因子,因此成为治疗CRC患者的有希望的药物靶标。
Emerging evidence showed that
FAT10 is a vital regulator of tumor occurrence and development. The molecular mechanisms underlying the specific role of
FAT10 in colorectal cancer (CRC) are not yet known.
To investigate whether
FAT10 participates in the proliferation, invasion and metastasis of CRC.
This study investigated the function and clinical significance of FAT10 protein expression in CRC. Furthermore, over-expression and knockdown experiments of FAT10 were developed to explore their effects on CRC cell migration and proliferation. Moreover, a molecular mechanism of
FAT10 regulate calpain small subunit 1(Capn4) was explored.
In this research, the FAT10 expression level was elevated in CRC tissues compared to corresponding normal tissues. In addition, the elevated FAT10 expression level is significantly linked to advanced clinical stage and poor CRC prognosis. Furthermore, a very high expression of
FAT10 was observed in CRC cells, and
FAT10 overexpression significantly enhanced the in vivo proliferation, invasion, and metastasis of the cells, whereas knockdown of FAT10 inhibited all these cellular factors in both in vivo and in vitro environments. Moreover, the outcomes of this study suggested that FAT10 enhances colorectal cancer progression through enhancement of Capn4 expression, leading to the progression of various human tumors, as reported by previous research. The mechanism via which FAT10 promotes CRC cells proliferation, invasion, and metastasis involves modification of the ubiquitination and degradation processes of Capn4.
FAT10 is a vital regulator of the tumorigenesis and advancement of CRC, thus serving as a promising pharmaceutical target for treating CRC patients.