Summary
Androgen/androgen receptor (AR) signaling plays important roles in normal
liver function and in progression of liver diseases. In studies of non-cancerous
liver diseases, AR knockout mouse models of liver disease have revealed that
androgen/AR signaling suppresses the development of steatosis, virus-related
hepatitis, and cirrhosis. In addition, studies have shown that targeting AR in
bone marrow-derived mesenchymal stem cells (BM-MSCs) improves their self-renewal
and migration potentials, thereby increasing the efficacy of BM-MSC
transplantation as a way to control the progression of cirrhosis. Androgen/AR
signaling is known to be involved in the initiation of carcinogen- or Hepatitis
B virus (HBV)-related hepatocellular carcinoma (HCC). However, studies have
demonstrated that AR, rather than androgen, plays the dominant role in cancer
initiation. Therefore, targeting AR might be an appropriate therapy for patients
with early-stage HCC. In contrast, androgen/AR signaling has been shown to
suppress metastasis of HCC in patients with late-stage disease. In addition,
there is evidence that therapy comprising Sorafenib and agents that enhance the
functional expression of AR may suppress the progression of late-stage HCC.