The androgen receptor (AR) can promote the formation of hepatocellular carcinoma (HCC) by regulating RNA replication of the hepatitis B virus (HBV). The research results showed that androgen receptors can affect the growth of hepatocellular carcinoma and the inhibition of the androgen receptors in liver cells by target is expected to be a method to assist in the treatment of liver cancer.

 

The results of this study have drawn considerable attention in the field of international research on hepatitis and liver cancer, and were published in the international authoritative medical journal Science Translational Medicine, and appeared on its cover. Science's publisher the American Association for the Advancement of Science (AAAS) called a press conference on May 20, 2010 in Washington, D. C. to reveal this breakthrough discovery.

 

Chronic hepatitis B virus infection is known to be an important factor in the cause of liver cancer.  The higher the amount of hepatitis B virus in the serum, the higher the incidence of developing hepatocellular carcinoma. In particular, male patients with hepatitis B are more prone to liver cancer than women. Furthermore, the chances of contracting liver cancer also greatly increase in male hepatitis B virus carriers if the androgen in the serum is higher or the activity of the androgen receptor is stronger. The evidence suggests that the androgen and its receptors may play an important role in the development of hepatocellular carcinoma caused by hepatitis B virus. However, no research has proved any of the correlation.

 

We used gene transfer technology to create the world's first hepatitis B laboratory mouse with androgen receptors removed from liver cells. Through the mice experiment, the androgen receptor did increase the replication of the hepatitis B virus and boost the incidence of liver cancer. Androgen receptor knockout mice with hepatitis B were less likely to suffer from liver cancer, with its incidence less than 7%, whereas those without the knockout had an incidence of over 47%, which proved that the male hormone receptor is associated with the formation of liver cancer.

 

Previous studies have shown that it is impossible to treat liver cancer effectively by lowering the androgen levels in the serum. Therefore, it may need to treat or control liver cancer by inhibiting the androgen receptors in the liver cells rather than reducing the androgen levels in the blood.

 

Our further study found that the androgen receptor may have different regulatory effects on liver cancer cells. In addition to inhibiting hepatoma cell invasion (metastasis), it also enhanced anoikis (apoptosis). Its function is multidirectional, and sometimes interfering with each other. The recent results were published in the international leading publication Journal of Hepatology of the July 2012 issue.

 

More and more knowledge tells us that the formation, differentiation, metastasis, and drug resistance of cancer are very complex. It is not possible to see the whole picture from a single or narrow perspective of a molecule (hormone) or a receptor. More efforts to integrate with different fields can enable us to have a slight and humble understanding of cancer.