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OCT4 increases BIRC5 and CCND1 expression and promotes cancer progression in hepatocellular carcinoma

Lu Cao1, Chunguang Li2, Shuwen Shen1, Yan Yan1, Weidan Ji1, Jinghan Wang1, Haihua Qian1, Xiaoqing Jiang1, Zhigang Li2, Mengchao Wu1, Ying Zhang3 and Changqing Su1*

Author affiliations

1 Department of Molecular Oncology, Eastern Hepatobiliary Surgical Hospital & Institute, Second Military Medical University, 200438, Shanghai, China

2 Department of Thoracic Surgery, Changhai Hospital, Second Military Medical University, 200438, Shanghai, China

3 Department of Pathology, Cancer Center of PLA, Nanjing 81 Hospital, 210002, Nanjing, China

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Citation and License

BMC Cancer 2013, 13:82  doi:10.1186/1471-2407-13-82

Published: 22 February 2013



OCT4 and BIRC5 are preferentially expressed in human cancer cells and mediate cancer cell survival and tumor maintenance. However, the molecular mechanism that regulates OCT4 and BIRC5 expression is not well characterized.


By manipulating OCT4 and BIRC5 expression in hepatocellular carcinoma (HCC) cell lines, the regulatory mechanism of OCT4 on BIRC5 and CCND1 were investigated.


Increasing or decreasing OCT4 expression could enhance or suppress BIRC5 expression, respectively, by regulating the activity of BIRC5 promoter. Because there is no binding site for OCT4 within BIRC5 promoter, the effect of OCT4 on BIRC5 promoter is indirect. An octamer motif for OCT4 in the CCND1 promoter has directly and partly participated in the regulation of CCND1 promoter activity, suggesting that OCT4 also could upregulated the expression of CCND1. Co-suppression of OCT4 and BIRC5 induced cancer cell apoptosis and cell cycle arrest, thereby efficiently inhibiting the proliferative activity of cancer cells and suppressing the growth of HCC xenogrfts in nude mice.


OCT4 can upregulate BIRC5 and CCND1 expression by increasing their promoter activity. These factors collusively promotes HCC cell proliferation, and co-suppression of OCT4 and BIRC5 is potentially beneficial for HCC treatment.

Transcription factor; Cell cycle; Cell apoptosis; Cancer biotherapy; Hepatocellular carcinoma