Tumor suppressor BLU inhibits proliferation of nasopharyngeal carcinoma cells by regulation of cell cycle, c-Jun N-terminal kinase and the cyclin D1 promoter
1 Department of Pathophysiology, Guangdong Medical College, 1 Xincheng Road, Song-Shan Lake (SSL) Science Technology and Industrial Park Dongguan, Guangdong, 523808, China
2 Key Laboratory for Medical Molecular Diagnostics of Guangdong Province Sino-American Cancer Research Institute, Guangdong Medical College, 1 Xincheng Road, Song-Shan Lake (SSL) Science, Technology and Industrial Park, Dongguan, Guangdong, 523808, China
3 State Key Laboratory of Oncology in South China, Department of Molecular Diagnostics, Sun Yat-sen University Cancer Center (SYSUCC), 651 Dong Feng Road, Guangzhou, Guangdong, 510060, China
BMC Cancer 2012, 12:267 doi:10.1186/1471-2407-12-267Published: 22 June 2012
Tumor suppressor genes function to regulate and block tumor cell proliferation. To explore the mechanisms underlying the tumor suppression of BLU/ZMYND10 gene on a frequently lost human chromosomal region, an adenoviral vector with BLU cDNA insert was constructed.
BLU was re-expressed in nasopharyngeal carcinoma cells by transfection or viral infection. Clonogenic growth was assayed; cell cycle was analyzed by flow cytometry-based DNA content detection; c-Jun N-terminal kinase (JNK) and cyclin D1 promoter activities were measured by reporter gene assay, and phosphorylation was measured by immunoblotting. The data for each pair of groups were compared with Student t tests.
BLU inhibits clonogenic growth of nasopharyngeal carcinoma cells, arrests cell cycle at G1 phase, downregulates JNK and cyclin D1 promoter activities, and inhibits phosphorylation of c-Jun.
BLU inhibits growth of nasopharyngeal carcinoma cells by regulation of the JNK-cyclin D1 axis to exert tumor suppression.