D-glucosamine inhibits proliferation of human cancer cells through inhibition of p70S6K.

Biochem Biophys Res Commun 2007 Sep 5;360(4):840-5. Epub 2007 Jul 5.

Chronic Disease Research Center and Institute for Medical Science, School of Medicine, Keimyung University, Daegu 700-712, Republic of Korea.

Although D-glucosamine has been reported as an inhibitor of tumor growth both in vivo and in vitro, the mechanism for the anticancer effect of D-glucosamine is still unclear. Since there are several reports suggesting D-glucosamine inhibits protein synthesis, we examined whether D-glucosamine affects p70S6K activity, an important signaling molecule involved in protein translation. In the present study, we found D-glucosamine inhibited the activity of p70S6K and the proliferation of DU145 prostate cancer cells and MDA-MB-231 breast cancer cells. D-glucosamine decreased phosphorylation of p70S6K, and its downstream substrates RPS6, and eIF-4B, but not mTOR and 4EBP1 in DU145 cells, suggesting that D-glucosamine induced inhibition of p70S6K is not through the inhibition of mTOR. In addition, D-glucosamine enhanced the growth inhibitory effects of rapamycin, a specific inhibitor of mTOR. These findings suggest that D-glucosamine can inhibit growth of cancer cells through dephosphorylation of p70S6K.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbrc.2007.06.137DOI Listing
September 2007

Publication Analysis

Top Keywords

cancer cells
16
d-glucosamine
10
inhibition p70s6k
8
suggesting d-glucosamine
8
d-glucosamine inhibits
8
p70s6k
6
cells
5
eif-4b mtor
4
d-glucosamine decreased
4
cells d-glucosamine
4
breast cancer
4
rps6 eif-4b
4
substrates rps6
4
mda-mb-231 breast
4
downstream substrates
4
phosphorylation p70s6k
4
decreased phosphorylation
4
p70s6k downstream
4
proliferation du145
4
study d-glucosamine
4

Similar Publications

D-glucosamine down-regulates HIF-1alpha through inhibition of protein translation in DU145 prostate cancer cells.

Biochem Biophys Res Commun 2009 Apr 28;382(1):96-101. Epub 2009 Feb 28.

Chronic Disease Research Center, School of Medicine, Keimyung University, 194 Dongsan-Dong, Jung-Gu, Daegu 700-712, Republic of Korea.

D-glucosamine has been reported to inhibit proliferation of cancer cells in culture and in vivo. In this study we report a novel response to D-glucosamine involving the translation regulation of hypoxia inducible factor (HIF)-1alpha expression. D-glucosamine caused a decreased expression of HIF-1alpha under normoxic and hypoxic conditions without affecting HIF-1alpha mRNA expression in DU145 prostate cancer cells. Read More

View Article and Full-Text PDF
April 2009

ET-18-OCH3 inhibits the phosphorylation and activation of p70 S6 kinase in MCF-7 cells.

Anticancer Res 2005 Jan-Feb;25(1A):95-100

Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, Manitoba, Canada R3E 0W3.

Alkyllysophospholipids (ALPs) inhibit the proliferation of epithelial cancer cells, and may achieve this by perturbing a number of intracellular signaling pathways. p70 S6 kinase (p70S6K) is a key intracellular signaling molecule in the regulation of cell proliferation. We therefore investigated whether ALPs inhibit p70S6K activity and, if so, whether this may be relevant in the mechanism of inhibition of cell proliferation by ALPs. Read More

View Article and Full-Text PDF
May 2005

RAD001 offers a therapeutic intervention through inhibition of mTOR as a potential strategy for esophageal cancer.

Oncol Rep 2010 Apr;23(4):1167-72

College of Life Science, Inner Mongolia University, The Key Laboratory of Mammal Reproductive Biology and Biotechnology, Ministry of Education, Hohhot 010021, PR China.

Esophageal cancer is one of the most frequently occurring cancers in the world. Targeting therapy strategy of cancer with specific inhibitors is developing and has showed promising antitumor efficacy. It is known that mTOR is an important controller of cell growth. Read More

View Article and Full-Text PDF
April 2010

Mammalian target of rapamycin inhibitors rapamycin and RAD001 (everolimus) induce anti-proliferative effects in GH-secreting pituitary tumor cells in vitro.

Endocr Relat Cancer 2009 Sep 9;16(3):1017-27. Epub 2009 Jun 9.

Institute of Endocrinology and Metabolism and Felsenstein Medical Research Center, Rabin Medical Center, Beilinson Campus, Petach Tikva 49100, Israel.

The effect of mammalian target of rapamycin (mTOR) inhibitors on pituitary tumors is unknown. Akt overexpression was demonstrated in pituitary adenomas, which may render them sensitive to the anti-proliferative effects of these drugs. The objective of the study was to evaluate the anti-proliferative efficacy of the mTOR inhibitor, rapamycin, and its orally bioavailable analog RAD001 on the GH-secreting pituitary tumor GH3 and MtT/S cells and in human GH-secreting pituitary adenomas (GH-omas) in primary cell cultures. Read More

View Article and Full-Text PDF
September 2009