TY - JOUR
T1 - Suppression of hormone-refractory prostate cancer by a novel nuclear factor κB inhibitor in nude mice
AU - Kikuchi, Eiji
AU - Horiguchi, Yutaka
AU - Nakashima, Jun
AU - Kuroda, Kenji
AU - Oya, Mototsugu
AU - Ohigashi, Takashi
AU - Takahashi, Nozomu
AU - Shima, Yutaka
AU - Umezawa, Kazuo
AU - Murai, Masaru
PY - 2003/1/1
Y1 - 2003/1/1
N2 - We have synthesized and explored the feasibility of using a novel nuclear factor (NF) κB inhibitor, a dehydroxymethylepoxyquinomicin designated as DHMEQ, against prostate cancer. The activity of NFκB, evaluated by transient transfection of a luciferase reporter DNA containing a specific binding sequence for NFκB, was inhibited by DHMEQ in three human hormone-refractory prostate cancer cell lines, DU145, JCA-1, and PC-3. Statistically significant growth inhibition was achieved by 20 μg/ml of DHMEQ, and marked levels of apoptosis were induced 48 h after DHMEQ administration in vitro. Electrophoretic mobility shift assay showed that DHMEQ completely inhibited NFκB DNA binding activity in JCA-1 cells. Furthermore, i.p. administrations of DHMEQ significantly inhibited pre-established JCA-1 s.c. tumor growth in nude mice without any side effects. Our result indicates the possibility of using a novel NFκB activation inhibitor, DHMEQ, as a new treatment strategy against hormone-refractory prostate cancer.
AB - We have synthesized and explored the feasibility of using a novel nuclear factor (NF) κB inhibitor, a dehydroxymethylepoxyquinomicin designated as DHMEQ, against prostate cancer. The activity of NFκB, evaluated by transient transfection of a luciferase reporter DNA containing a specific binding sequence for NFκB, was inhibited by DHMEQ in three human hormone-refractory prostate cancer cell lines, DU145, JCA-1, and PC-3. Statistically significant growth inhibition was achieved by 20 μg/ml of DHMEQ, and marked levels of apoptosis were induced 48 h after DHMEQ administration in vitro. Electrophoretic mobility shift assay showed that DHMEQ completely inhibited NFκB DNA binding activity in JCA-1 cells. Furthermore, i.p. administrations of DHMEQ significantly inhibited pre-established JCA-1 s.c. tumor growth in nude mice without any side effects. Our result indicates the possibility of using a novel NFκB activation inhibitor, DHMEQ, as a new treatment strategy against hormone-refractory prostate cancer.
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UR - http://www.scopus.com/inward/citedby.url?scp=0037227989&partnerID=8YFLogxK
M3 - Article
C2 - 12517785
AN - SCOPUS:0037227989
VL - 63
SP - 107
EP - 110
JO - Journal of Cancer Research
JF - Journal of Cancer Research
SN - 0008-5472
IS - 1
ER -
