RT Journal Article
SR Electronic
T1 Targeting PI3KC2β Impairs Proliferation and Survival in Acute Leukemia, Brain Tumours and Neuroendocrine Tumours
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 3015
OP 3027
VO 32
IS 8
A1 DANIELLE BOLLER
A1 KATHRIN T. DOEPFNER
A1 ANGELA DE LAURENTIIS
A1 ANA S. GUERREIRO
A1 MARIN MARINOV
A1 TAREK SHALABY
A1 PAUL DEPLEDGE
A1 ANTHONY ROBSON
A1 NAHID SAGHIR
A1 MASAHIKO HAYAKAWA
A1 HIROYUKI KAIZAWA
A1 TOMONOBU KOIZUMI
A1 TAKAHIDE OHISHI
A1 SARAH FATTET
A1 OLIVIER DELATTRE
A1 ANELIA SCHWERI-OLAC
A1 KATRIN HÖLAND
A1 MICHAEL A. GROTZER
A1 KARL FREI
A1 OLIVIER SPERTINI
A1 MICHAEL D. WATERFIELD
A1 ALEXANDRE ARCARO
YR 2012
UL http://ar.iiarjournals.org/content/32/8/3015.abstract
AB Background: Eight human catalytic phosphoinositide 3-kinase (PI3K) isoforms exist which are subdivided into three classes. While class I isoforms have been well-studied in cancer, little is known about the functions of class II PI3Ks. Materials and Methods: The expression pattern and functions of the class II PI3KC2β isoform were investigated in a panel of tumour samples and cell lines. Results: Overexpression of PI3KC2β was found in subsets of tumours and cell lines from acute myeloid leukemia (AML), glioblastoma multiforme (GBM), medulloblastoma (MB), neuroblastoma (NB), and small cell lung cancer (SCLC). Specific pharmacological inhibitors of PI3KC2β or RNA interference impaired proliferation of a panel of human cancer cell lines and primary cultures. Inhibition of PI3KC2β also induced apoptosis and sensitised the cancer cells to chemotherapeutic agents. Conclusion: Together, these data show that PI3KC2β contributes to proliferation and survival in AML, brain tumours and neuroendocrine tumours, and may represent a novel target in these malignancies.