Overexpressed ubiquitin ligase Cullin7 in breast cancer promotes cell proliferation and invasion via down-regulating p53
- Department of Histology and Embryology, Guangdong Medical College, Dongguan 523808, Guangdong (China)
- The 7th People’s Hospital of Chengdu, Chengdu 610041, Sichuan (China)
- The Second School of Clinical Medicine, Guangdong Medical College, Dongguan 523808, Guangdong (China)
- School of Pharmacy, Guangdong Medical College, Dongguan 523808, Guangdong (China)
- Oncology of Affiliated Hospital Guangdong Medical College, Zhanjiang 524000, Guangdong (China)
Highlights: • Cullin7 is overexpressed in human breast cancer samples. • Cullin7 stimulated proliferation and invasion of breast cancer cells. • Inhibition of p53 contributes to Cullin7-induced proliferation and invasion. - 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.
- OSTI ID:
- 22416687
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 450, Issue 4; Other Information: Copyright (c) 2014 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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