TY - JOUR
T1 - Alterations of metastasis-related genes identified using an oligonucleotide microarray of genistein-treated HCC1395 breast cancer cells
AU - Lee, Wen Ying
AU - Huang, Soon Cen
AU - Tzeng, Ching Cherng
AU - Chang, Tsui Ling
AU - Hsu, Keng Fu
N1 - Funding Information:
This work is supported by grants from the National Science Council (92-2320-B-006-072, NSC 93-2320-B-384-003, 94-2320-B-384-001) and Chi Mei Medical Center (CMNSC-9304, CMNSC-9403), Taiwan. Address correspondence to Wen-Ying Lee, Department of Pathology, Chi Mei Medical Center, 901 Chung Hwa Road, Tainan 710, Taiwan. Phone: 886-6-281-2811. FAX: 886-6-274-6411. E-mail: [email protected].
PY - 2007
Y1 - 2007
N2 - Genistein, one of the major isoflavones, potently inhibits the growth and metastasis of breast cancer. However, the precise molecular mechanism in metastasis inhibition is not clear. We investigated the effect of genistein in HCC1395 cells, a cell line derived from an early-stage primary breast cancer. Genistein dose dependently both decreased cell viability and inhibited the invasion potential. We used human oligonucleotide microarrays to determine the gene expression profile altered by genistein treatment. TFP1-2, ATF3, DNMT1, and MTCBP-1, which inhibit invasion and metastasis, were upregulated, and MMP-2, MMP-7, and CXCL12, which promote invasion and metastasis, were downregulated. We used quantitative real-time polymerase chain reaction to verify the microarray data at the mRNA level. We conclude that genistein-induced alternations of gene expression involving metastasis may be exploited for devising chemopreventive and therapeutic strategies, particularly for early-stage breast cancer.
AB - Genistein, one of the major isoflavones, potently inhibits the growth and metastasis of breast cancer. However, the precise molecular mechanism in metastasis inhibition is not clear. We investigated the effect of genistein in HCC1395 cells, a cell line derived from an early-stage primary breast cancer. Genistein dose dependently both decreased cell viability and inhibited the invasion potential. We used human oligonucleotide microarrays to determine the gene expression profile altered by genistein treatment. TFP1-2, ATF3, DNMT1, and MTCBP-1, which inhibit invasion and metastasis, were upregulated, and MMP-2, MMP-7, and CXCL12, which promote invasion and metastasis, were downregulated. We used quantitative real-time polymerase chain reaction to verify the microarray data at the mRNA level. We conclude that genistein-induced alternations of gene expression involving metastasis may be exploited for devising chemopreventive and therapeutic strategies, particularly for early-stage breast cancer.
UR - https://www.scopus.com/pages/publications/34548237679
UR - https://www.scopus.com/pages/publications/34548237679#tab=citedBy
U2 - 10.1080/01635580701328636
DO - 10.1080/01635580701328636
M3 - Article
C2 - 17640171
AN - SCOPUS:34548237679
SN - 0163-5581
VL - 58
SP - 239
EP - 246
JO - Nutrition and Cancer
JF - Nutrition and Cancer
IS - 2
ER -