INPP4B-mediated tumor resistance is associated with modulation of glucose metabolism via hexokinase 2 regulation in laryngeal cancer cells.

Abstract	Inositol polyphosphate 4-phosphatase type II (INPP4B) was recently identified as a tumor resistance factor in laryngeal cancer cells. Herein, we show that INPP4B-mediated resistance is associated with increased glycolytic phenotype. INPP4B expression was induced by hypoxia and irradiation. Intriguingly, overexpression of INPP4B enhanced aerobic glycolysis. Of the glycolysis-regulatory genes, hexokinase 2 (HK2) was mainly regulated by INPP4B and this regulation was mediated through the Akt-mTOR pathway. Notably, codepletion of INPP4B and HK2 markedly sensitized radioresistant laryngeal cancer cells to irradiation or anticancer drug. Moreover, INPP4B was significantly associated with HK2 in human laryngeal cancer tissues. Therefore, these results suggest that INPP4B modulates aerobic glycolysis via HK2 regulation in radioresistant laryngeal cancer cells.
Authors	Joong Won Min, Kwang Il Kim, Hyun-Ah Kim, Eun-Kyu Kim, Woo Chul Noh, Hong Bae Jeon, Dong-Hyung Cho, Jeong Su Oh, In-Chul Park, Sang-Gu Hwang, Jae-Sung Kim
Journal	Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 440 Issue 1 Pg. 137-42 (Oct 11 2013) ISSN: 1090-2104 [Electronic] United States
PMID	24051093 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright	Copyright © 2013 Elsevier Inc. All rights reserved.
Chemical References	Antineoplastic Agents Hypoxia-Inducible Factor 1, alpha Subunit Hexokinase MTOR protein, human Proto-Oncogene Proteins c-akt TOR Serine-Threonine Kinases Phosphoric Monoester Hydrolases phosphatidylinositol-3,4-bisphosphate 4-phosphatase Glucose
Topics	Antineoplastic Agents (pharmacology) Cell Line, Tumor Drug Resistance, Neoplasm Glucose (metabolism) Glycolysis Hexokinase (genetics, metabolism) Humans Hypoxia-Inducible Factor 1, alpha Subunit (genetics, metabolism) Laryngeal Neoplasms (drug therapy, genetics, pathology, radiotherapy) Larynx (drug effects, metabolism, pathology, radiation effects) Phosphoric Monoester Hydrolases (genetics, metabolism) Proto-Oncogene Proteins c-akt (metabolism) RNA Interference TOR Serine-Threonine Kinases (metabolism)

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