Ablation of phosphoinositide-3-kinase class II alpha suppresses hepatoma cell proliferation |
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Authors: | Stanley K.L. Ng Soek-Ying Neo Yann-Wan Yap Evelyn S.L. Loh Ee-Chee Ren |
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Affiliation: | a Singapore Immunology Network A∗STAR, Singapore b Genome Institute of Singapore A∗STAR, Singapore c Department of General Surgery, Tan Tock Seng Hospital, Singapore d Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore |
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Abstract: | Cancer such as hepatocellular carcinoma (HCC) is characterized by complex perturbations in multiple signaling pathways, including the phosphoinositide-3-kinase (PI3K/AKT) pathways. Herein we investigated the role of PI3K catalytic isoforms, particularly class II isoforms in HCC proliferation. Among the siRNAs tested against the eight known catalytic PI3K isoforms, specific ablation of class II PI3K alpha (PIK3C2α) was the most effective in impairing cell growth and this was accompanied by concomitant decrease in PIK3C2α mRNA and protein levels. Colony formation ability of cells deficient for PIK3C2α was markedly reduced and growth arrest was associated with increased caspase 3 levels. A small but significant difference in gene dosage and expression levels was detected between tumor and non-tumor tissues in a cohort of 19 HCC patients. Taken together, these data suggest for the first time that in addition to class I PI3Ks in cancer, class II PIK3C2α can modulate HCC cell growth. |
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Keywords: | HCC, hepatocellular carcinoma PI3K, phosphoinositide-3-kinase PIK3C2α, phosphoinositide-3-kinase class 2 alpha |
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