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乳腺癌中过表达的泛素连接酶Cullin7通过下调p53促进细胞增殖和侵袭。

Overexpressed ubiquitin ligase Cullin7 in breast cancer promotes cell proliferation and invasion via down-regulating p53.

作者信息

Guo Hongsheng, Wu Fenping, Wang Yan, Yan Chong, Su Wenmei

机构信息

Department of Histology and Embryology, Guangdong Medical College, Dongguan 523808, Guangdong, China.

The 7th People's Hospital of Chengdu, Chengdu 610041, Sichuan, China.

出版信息

Biochem Biophys Res Commun. 2014 Aug 8;450(4):1370-6. doi: 10.1016/j.bbrc.2014.06.134. Epub 2014 Jul 5.

Abstract

Ubiquitin ligase Cullin7 has been identified as an oncogene in some malignant diseases such as choriocarcinoma and neuroblastoma. However, the role of Cullin7 in breast cancer carcinogenesis remains unclear. In this study, we compared Cullin7 protein levels in breast cancer tissues with normal breast tissues and identified significantly higher expression of Cullin7 protein in breast cancer specimens. By overexpressing Cullin7 in breast cancer cells HCC1937, we found that Cullin7 could promote cell growth and invasion in vitro. In contrast, the cell growth and invasion was inhibited by silencing Cullin7 in breast cancer cell BT474. Moreover, we demonstrated that Cullin7 promoted breast cancer cell proliferation and invasion via down-regulating p53 expression. Thus, our study provided evidence that Cullin7 functions as a novel oncogene in breast cancer and may be a potential therapeutic target for breast cancer management.

摘要

泛素连接酶Cullin7已被确定为某些恶性疾病(如绒毛膜癌和神经母细胞瘤)中的一种癌基因。然而,Cullin7在乳腺癌发生中的作用仍不清楚。在本研究中,我们比较了乳腺癌组织和正常乳腺组织中Cullin7蛋白水平,发现乳腺癌标本中Cullin7蛋白表达明显更高。通过在乳腺癌细胞HCC1937中过表达Cullin7,我们发现Cullin7可促进体外细胞生长和侵袭。相反,在乳腺癌细胞BT474中沉默Cullin7可抑制细胞生长和侵袭。此外,我们证明Cullin7通过下调p53表达促进乳腺癌细胞增殖和侵袭。因此,我们的研究提供了证据表明Cullin7在乳腺癌中作为一种新的癌基因发挥作用,可能是乳腺癌治疗的潜在靶点。

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