RRC ID 62258
著者 Noguchi C, Kamitori K, Hossain A, Hoshikawa H, Katagi A, Dong Y, Sui L, Tokuda M, Yamaguchi F.
タイトル D-Allose Inhibits Cancer Cell Growth by Reducing GLUT1 Expression.
ジャーナル Tohoku J Exp Med
Abstract Glucose is a major energy source for mammalian cells and is transported into cells via cell-specific expression of various glucose transporters (GLUTs). Especially, cancer cells require massive amounts of glucose as an energy source for their dysregulated growth and thus over-express GLUTs. d-allose, a C-3 epimer of d-glucose, is one of rare sugars that exist in small quantities in nature. We have shown that d-allose induces the tumor suppressor gene coding for thioredoxin interacting protein (TXNIP) and inhibits cancer cell growth by G1 cell cycle arrest. It has also been reported that GLUTs including GLUT1 are over-expressed in many cancer cell lines, which may contribute to larger glucose utilization. Since d-allose suppresses the growth of cancer cells through the upregulation of TXNIP expression, our present study focused on whether d-allose down-regulates GLUT1 expression via TXNIP expression and thus suppresses cancer cell growth. Western blot and real-time PCR analyses revealed that d-allose significantly induced TXNIP expression and inhibited GLUT1 expression in a dose-dependent manner in three human cancer cell lines: hepatocellular carcinoma (HuH-7), Caucasian breast adenocarcinoma (MDA-MB-231), and neuroblastoma (SH-SY5Y). In these cell lines, d-allose treatment inhibited cell growth. Importantly, d-allose treatment decreased glucose uptake, as measured by the uptake of 2-deoxy d-glucose. Moreover, the reporter assays showed that d-allose decreased the expression of luciferase through the hypoxia response element present in the tested promoter region. These results suggest that d-allose may cause the inhibition of cancer growth by reducing both GLUT1 expression and glucose uptake.
巻・号 238(2)
ページ 131-41
公開日 2016-2-1
DOI 10.1620/tjem.238.131
PMID 26829886
MeSH Carrier Proteins / genetics Carrier Proteins / metabolism Cell Line, Tumor Cell Proliferation / drug effects Down-Regulation / drug effects Gene Expression Regulation, Neoplastic / drug effects Gene Knockdown Techniques Glucose / metabolism Glucose / pharmacology* Glucose Transporter Type 1 / genetics* Glucose Transporter Type 1 / metabolism Humans Neoplasms / genetics* Neoplasms / pathology* RNA, Messenger / genetics RNA, Messenger / metabolism Response Elements Up-Regulation / drug effects
IF 1.441
リソース情報
ヒト・動物細胞 HuH-7