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Cullin7 Is Required for Lung Cancer Cell Proliferation and Is Overexpressed in Lung Cancer

机译:Cullin7是肺癌细胞增殖所必需的,在肺癌中过表达

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Ubiquitin ligase Cullin7 has been identified as an oncogene in some malignant diseases such as choriocarcinoma and neuroblastoma. However, the role of Cullin7 in lung cancer carcinogenesis remains unclear. In this study, we explored the functional role of Cullin7 in lung cancer cell proliferation and tumorigenesis and determined its expression profile in lung cancer. Knocking down Cullin7 expression by small interfering RNA (siRNA) in lung cancer cells inhibited cell proliferation and elevated the expression of p53, p27, and p21 proteins. The enhanced p53 expression resulted from activation of the DNA damage response pathway. Cullin7 knockdown markedly suppressed xenograft tumor growth in vivo in mice. Moreover, Cullin7 expression was increased in primary lung cancer tissues of humans. Thus, Cullin7 is required for sustained proliferation and survival of tumor cells in vitro and in vivo, and its aberrant expression may contribute to the pathogenesis of lung cancer. Thus, our study provided evidence that Cullin7 functions as a novel oncogene in lung cancer and may be a potential therapeutic target for lung cancer management.
机译:泛素连接酶Cullin7已被确定为绒癌和神经母细胞瘤等某些恶性疾病的致癌基因。但是,Cullin7在肺癌致癌作用中的作用仍不清楚。在这项研究中,我们探讨了Cullin7在肺癌细胞增殖和肿瘤发生中的功能,并确定了其在肺癌中的表达情况。在肺癌细胞中通过小干扰RNA(siRNA)抑制Cullin7的表达抑制细胞增殖并提高p53,p27和p21蛋白的表达。 p53表达的增强是由于DNA损伤反应途径的激活所致。 Cullin7敲低显着抑制了小鼠体内异种移植肿瘤的生长。而且,在人的原发性肺癌组织中Cullin7表达增加。因此,Cullin7是肿瘤细胞在体外和体内持续增殖和存活所必需的,其异常表达可能有助于肺癌的发病机理。因此,我们的研究提供了证据,表明Cullin7在肺癌中起新型致癌基因的作用,并且可能成为肺癌治疗的潜在治疗靶标。

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