Sulforaphane inhibits the proliferation of the BIU87 bladder cancer cell line via IGFBP-3 elevation

• Published in: Asian Pacific journal of cancer prevention : APJCP Vol. 15; no. 4; pp. 1517 - 1520
• Main Authors: Dang, Ya-Mei, Huang, Gang, Chen, Yi-Rong, Dang, Zhong-Feng, Chen, Cheng, Liu, Feng-Lei, Guo, Ying-Fang, Xie, Xiao-Dong
• Format: Journal Article
• Language: English
• Published: Thailand 01-01-2014
• Subjects: Anticarcinogenic Agents - pharmacology; Apoptosis; Cell Line, Tumor; Cell Proliferation - drug effects; Humans; Insulin-Like Growth Factor Binding Protein 3 - biosynthesis; Insulin-Like Growth Factor Binding Protein 3 - genetics; Isothiocyanates - pharmacology; M Phase Cell Cycle Checkpoints - drug effects; NF-kappa B - biosynthesis; NF-kappa B - genetics; RNA Interference; RNA, Messenger - biosynthesis; RNA, Small Interfering; Signal Transduction - drug effects; Urinary Bladder Neoplasms - drug therapy
• ISSN: 1513-7368; 2476-762X
• DOI: 10.7314/APJCP.2014.15.4.1517

To investigate effects of sulforaphane on the BIU87 cell line and underlying mechanisms involving IGFBP-3.
Both BIU87 and IGFBP-3-silenced BIU87 cells were treated with sulforaphane. Cell proliferation was detected by MTT assay. Cell cycle and apoptosis were determined via flow cytometry. Quantitative polymerase chain reaction and Western blotting were applied to analyze the expression of IGFBP-3 and NF-κB at both mRNA and protein levels.
Sulforaphane (80 μM) treatment could inhibit cell proliferation, inducing apoptosis and cell cycle arrest at G2/M phase. All these effects could be antagonized by IGFBP-3 silencing. Furthermore, sulforaphane (80 μM) could down-regulate NF-κB expression while elevating that of IGFBP-3.
Sulforaphane could suppress the proliferation of BIU87 cells via enhancing IGFBP-3 expression, which negatively regulating the NF-κB signaling pathway.