@article{oai:repo.qst.go.jp:00044877,
 author = {Niina, Ichiro and Uchiumi, Takeshi and Izumi, Hiroto and Torigoe, Takayuki and Wakasugi, Tetsuro and Igarashi, Tomonori and Miyamoto, Naoya and Onitsuka, Takamitsu and Shiota, Masaki and Okayasu, Ryuichi and Chijiiwa, Kazuo and Kohno, Kimitoshi and 岡安 隆一},
 issue = {6},
 journal = {Cancer Science},
 month = {Apr},
 note = {Modification of transcription factors by anti-cancer agents plays an important role inboth apoptotic and survival signaling. Here we report that both DNA topoisomerase Iand II inhibitors such as SN-38 and etoposide, but not cisplatin, 5-fluorouracil or
actinomycin D, can induce phosphorylation of the transcription factor Sp1. Furthermore,DNA topoisomerase inhibitors were shown to transactivate GC-box-dependent promoters such as the SV40 and VEGF promoters. The phosphorylated form of Sp1 was detectable within 30 minutes of inhibitor treatment and was greatly diminished by the presence of the PI3K inhibitor wortmannin and by DNA-dependent protein kinase (DNA-PK) knockdown. We also confirmed that the phosphorylated form of DNA-PK was increased by treatment with both etoposide and SN-38. Taken together, these findings demonstrate a novel genomic response to anticancer agents that induce Sp1 phosphorylation, and might contribute to tumor progression and drug resistance.},
 pages = {858--863},
 title = {DNA topoisomerase inhibitor, etoposide, enhances GC-box-dependent promoter activity via Sp1 phosphorylation},
 volume = {98},
 year = {2007}
}