PMID- 25071315
OWN - NLM
STAT- MEDLINE
DCOM- 20150417
LR  - 20211203
IS  - 2219-2840 (Electronic)
IS  - 1007-9327 (Print)
IS  - 1007-9327 (Linking)
VI  - 20
IP  - 28
DP  - 2014 Jul 28
TI  - Androgen receptor signaling in hepatocellular carcinoma and pancreatic cancers.
PG  - 9229-36
LID - 10.3748/wjg.v20.i28.9229 [doi]
AB  - Hepatocellular carcinoma (HCC) and pancreatic cancer remain difficult to treat, 
      and despite the ongoing development of new treatments, the overall survival rate 
      has only modestly improved over the past decade. Liver and pancreatic progenitors 
      commonly develop from endoderm cells in the embryonic foregut. A previous study 
      showed that HCC and pancreatic cancer cell lines variably express androgen 
      receptor (AR), and these cancers and the surrounding tissues also express AR. AR 
      is a ligand-dependent transcription factor that belongs to the nuclear receptor 
      superfamily. Androgen response element is present in regulatory elements on the 
      AR-responsive target genes, such as transforming growth factor beta-1 (TGF 
      beta-1) and vascular endothelial growth factor (VEGF). It is well known that the 
      activation of AR is associated with human carcinogenesis in prostate cancer as 
      well as HCC and pancreatic cancer and that GRP78, TGF beta, and VEGF all play 
      important roles in carcinogenesis and cancer development in these cancers. HCC is 
      a male-dominant cancer irrespective of its etiology. Previous work has reported 
      that vertebrae forkhead box A 1/2 are involved in estrogen receptors and/or AR 
      signaling pathways, which may contribute to the gender differences observed with 
      HCC. Our recent work also showed that AR has a critical role in pancreatic cancer 
      development, despite pancreatic cancer not being a male dominant cancer. Aryl 
      hydrocarbon (or dioxin) receptor is also involved in both HCC and pancreatic 
      cancer through the formation of complex with AR. It is possible that AR might be 
      involved in their carcinogenesis through major histocompatibility complex 
      class I chain-related gene A/B. This review article describes AR and its role in 
      HCC and pancreatic cancer and suggests that more specific AR signaling-inhibitors 
      may be useful in the treatment of these "difficult to treat" cancers.
FAU - Kanda, Tatsuo
AU  - Kanda T
AD  - Tatsuo Kanda, Xia Jiang, Osamu Yokosuka, Department of Gastroenterology and 
      Nephrology, Chiba University, Graduate School of Medicine, Chiba 260-8677, Japan.
FAU - Jiang, Xia
AU  - Jiang X
AD  - Tatsuo Kanda, Xia Jiang, Osamu Yokosuka, Department of Gastroenterology and 
      Nephrology, Chiba University, Graduate School of Medicine, Chiba 260-8677, Japan.
FAU - Yokosuka, Osamu
AU  - Yokosuka O
AD  - Tatsuo Kanda, Xia Jiang, Osamu Yokosuka, Department of Gastroenterology and 
      Nephrology, Chiba University, Graduate School of Medicine, Chiba 260-8677, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - World J Gastroenterol
JT  - World journal of gastroenterology
JID - 100883448
RN  - 0 (Androgen Receptor Antagonists)
RN  - 0 (Antineoplastic Agents, Hormonal)
RN  - 0 (Endoplasmic Reticulum Chaperone BiP)
RN  - 0 (HSPA5 protein, human)
RN  - 0 (Receptors, Androgen)
SB  - IM
MH  - Androgen Receptor Antagonists/therapeutic use
MH  - Animals
MH  - Antineoplastic Agents, Hormonal/therapeutic use
MH  - Carcinoma, Hepatocellular/drug therapy/*metabolism/pathology
MH  - Endoplasmic Reticulum Chaperone BiP
MH  - Humans
MH  - Liver Neoplasms/drug therapy/*metabolism/pathology
MH  - Molecular Targeted Therapy
MH  - Pancreatic Neoplasms/drug therapy/*metabolism/pathology
MH  - Receptors, Androgen/drug effects/*metabolism
MH  - *Signal Transduction/drug effects
PMC - PMC4110552
OTO - NOTNLM
OT  - Androgen receptor
OT  - Gender difference
OT  - Hepatocellular carcinoma
OT  - Male-dominant
OT  - Pancreas
EDAT- 2014/07/30 06:00
MHDA- 2015/04/18 06:00
PMCR- 2014/07/28
CRDT- 2014/07/30 06:00
PHST- 2014/01/17 00:00 [received]
PHST- 2014/03/07 00:00 [revised]
PHST- 2014/04/30 00:00 [accepted]
PHST- 2014/07/30 06:00 [entrez]
PHST- 2014/07/30 06:00 [pubmed]
PHST- 2015/04/18 06:00 [medline]
PHST- 2014/07/28 00:00 [pmc-release]
AID - 10.3748/wjg.v20.i28.9229 [doi]
PST - ppublish
SO  - World J Gastroenterol. 2014 Jul 28;20(28):9229-36. doi: 10.3748/wjg.v20.i28.9229.