PT  - JOURNAL ARTICLE
AU  - SHINJI MIWA
AU  - NAOTOSHI SUGIMOTO
AU  - NORIO YAMAMOTO
AU  - TOSHIHARU SHIRAI
AU  - HIDEJI NISHIDA
AU  - KATSUHIRO HAYASHI
AU  - HIROAKI KIMURA
AU  - AKIHIKO TAKEUCHI
AU  - KENTARO IGARASHI
AU  - AKIHIRO YACHIE
AU  - HIROYUKI TSUCHIYA
TI  - Caffeine Induces Apoptosis of Osteosarcoma Cells by Inhibiting AKT/mTOR/S6K, NF-κB and MAPK Pathways
DP  - 2012 Sep 01
TA  - Anticancer Research
PG  - 3643--3649
VI  - 32
IP  - 9
4099  - http://ar.iiarjournals.org/content/32/9/3643.short
4100  - http://ar.iiarjournals.org/content/32/9/3643.full
SO  - Anticancer Res2012 Sep 01; 32
AB  - We previously reported that caffeine-assisted chemotherapy improved the treatment of malignant bone and soft tissue tumours such as osteosarcoma. Caffeine affects tumour cells through various pathways, including phosphatase and tensin homolog deleted on chromosome 10 (PTEN), AKT, Bcl-2–associated X protein (BAX), caspase-3 and p53, and has therefore been indicated as being useful for the treatment of malignant tumours. Here, the effects of caffeine on the proliferation of HOS osteosarcoma cells were assessed by WST-8 assay, and the effects on the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK) pathways were assessed by western blot analyses. Caffeine inhibited proliferation of HOS cells and suppressed NF-κB, AKT, mTOR/S6K and ERK activities. Our results support those from previous studies relating to the use of caffeine in the treatment of osteosarcoma.