1Centre
for Biotechnology, Institute of Science and Technology,
Jawaharlal Nehru Technological University, Hyderabad,
2Department of Biotechnology, Chaitanya
Bharathi Institute of Technology, Hyderabad, India.
*Corresponding
author: E-mail:
narasu.lakshmi@yahoo.com
Received: 7 August
2008
Revised accepted: 15 October 2008
Tropical
Journal of Pharmaceutical Research, February
2009; 8(1):
3-9
Abstract
Purpose: CD133 (prominin-1), a 5-transmembrane
glycoprotein, has recently been considered an important
marker that represents the subset population of cancer
stem-like cells. The purpose of the present study is to
isolate cancerous stem-like cells from normal healthy
volunteers and prostate cancer patients (CD133+)
which also express MDR1 and to ascertain the influence
of Oct-4 on ‘stem-ness’ and differentiation of these
CD133+ cells towards epithelium.
Methods: CD133+ cells were isolated
using magnetic beads from normal healthy volunteers and
prostate cancer patients (NV-CD133+and
PC-CD133+). The isolated cells were analyzed
using flow cytometry and Western blot technique for
CD133, MDR1 and Oct-4. CD133+MDR1+
cells were cultured in presence and absence of antihuman
Oct-4 blocking antibody.
Results: PC-CD133+ cells displayed
higher Oct-4 expression with the ability to self-renew
and may represent a reservoir with differentiation
potential for generating prostate cancer cells.
Furthermore, PC-CD133+ cells highly
co-expressed the multiple drug-resistant marker MDR1.
The treatment with Oct-4 blocking antibody can
specifically block the capability of PC-CD133+
cells to differentiate into prostate epithelial cells
bearing CD57.
Conclusion: PC-CD133+ cells displayed
a higher Oct-4 expression with the ability to self-renew
and may represent a reservoir with differentiation
potentials for progression of prostate cancer. The MDR1
expression of PC-CD133+ cells in vitro and in
vivo is partially due to preferential activation of
Oct-4 gene expression.
Keywords:
Prostate cancer, Cancer stem-like cells, Oct-4, CD133,
Multi-drug resistance1 (MDR1)