Nuclear factor-kappa B inhibition reduces markedly cell proliferation in Epstein-Barr virus-infected stomach cancer, but affects variably in Epstein-Barr virus-negative stomach cancer.
Nuclear factor-kappa B (NF-kappaB) inhibition by NF-kappaB p65-specific siRNA induced a near-cessation of cell proliferation in EBV-positive stomach cancer cell, and notably diminished cell proliferation in EBV- positive Raji lymphoma cell. In EBV-negative stomach cancer cells, NF-kappaB inhibition affected variably cell proliferation. Regardless of cell type, NF-kappaB inhibition suppressed antiapoptotic function of NF-kappaB, and tended to promote the nuclear accumulation of beta-catenin. This inverse relationship between NF-kappaB and beta-catenin was evident in 120 resected gastric carcinomas. Conclusively, NF-kappaB inhibition may be beneficial in the therapy of EBV-positive stomach cancer, but influence variously EBV-negative stomach cancer.
Jeong
Jin-Yong
JY
Center for Antimicrobial Resistance and Microbial Genetics, Department of Infectious Diseases, University of Ulsan College of Medicine, Seoul 138-736, Korea.
Woo
Jun Hee
JH
Kim
Yang Soo
YS
Choi
Sangho
S
Lee
Sang Oh
SO
Kil
Seol-Ryoung
SR
Kim
Chul Woo
CW
Lee
Byung Lan
BL
Kim
Woo Ho
WH
Nam
Byung-Ho
BH
Chang
Mee Soo
MS
D000818:Animals; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D004854:Herpesvirus 4, Human; D006801:Humans; D016328:NF-kappa B / Q000037:antagonists & inhibitors*; D013274:Stomach Neoplasms / Q000821:virology; D014162:Transfection; D051176:beta Catenin / Q000378:metabolism
D016328:NF-kappa B; D051176:beta Catenin