Stromal-epithelial interaction in prostate cancer progression.
Cancer is not a single-cell disease, and its existence and behavior are constantly modulated by the host. Cancer gene expression and genetics are also highly dynamic and are regulated epigenetically by the host through gene-environment interaction. In this article, we describe the molecular pathways leading to an unusual property of cancer cells: the ability to mimic the host microenvironment and, in particular, the characteristics of osteomimicry and vasculogenic mimicry, which are likely to be regulated by soluble and insoluble factors in the tumor-adjacent microenvironment. We also discuss the importance of host inflammatory and stem cells that contribute to the growth and survival of cancer cells. By understanding the salient features of cancer-host interaction, novel therapeutics might be developed to target the cancer and its host in the treatment of lethal prostate cancer metastases.
Chung
Leland W K
LW
Molecular Urology and Therapeutics Program, Department of Urology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA. lwchung@emory.edu
Huang
Wen-Chin
WC
Sung
Shian-Ying
SY
Wu
Daqing
D
Odero-Marah
Valerie
V
Nomura
Takeo
T
Shigemura
Katsumi
K
Miyagi
Tohru
T
Seo
Seogil
S
Shi
Chumeng
C
Molitierno
Joe
J
Elmore
James
J
Anderson
Cynthia
C
Isotani
Shuji
S
Edlund
Magnus
M
Hsieh
Chia-Ling
CL
Wang
Ruoxiang
R
Shehata
Bahig
B
Zhau
Haiyen E
HE
D014408:Biomarkers, Tumor; D002450:Cell Communication; D018450:Disease Progression; D004847:Epithelial Cells / Q000473:pathology*; D005109:Extracellular Matrix / Q000378:metabolism; D006801:Humans; D008297:Male; D011471:Prostatic Neoplasms / Q000503:physiopathology*; D017154:Stromal Cells / Q000473:pathology*
D014408:Biomarkers, Tumor