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INPP4B is an oncogenic regulator in human colon cancer

by Guo, S T , Zhang, X D , Agoulnik, I U , Thorne, R F , Liu, T , Wang, F H , Jin, L , Lai, F , Zan, L K , Yang, R H , Farrelly, M , Guo, X Y , Croft, A , Hondermarck, H , Yan, X G , Scott, R , Ackland, S , Xi, Y F , Tseng, H-Y , Wang, J F , Wang, C Y , Li, Y P , Chi, M N , Jiang, C C

in 13/51 / 13/95 / 14/105 / 38/109 / 38/61 / 38/77 / 38/89 / 45/22 / 45/77 / 631/67/1504/1885 / 631/67/1504/2330 / 64/60 / 82/1 / 96/95 / Apoptosis / Cell Biology / Cell growth / Cell Line, Tumor / Cell Proliferation - genetics / Colon cancer / Colonic Neoplasms - genetics / Colonic Neoplasms - metabolism / Colonic Neoplasms - pathology / Colorectal cancer / Development and progression / Gene expression / Gene silencing / Genetic aspects / Health aspects / Human Genetics / Humans / Immunohistochemistry / Internal Medicine / Kinases / Medicine / Medicine & Public Health / Oncology / Original / original-article / Phosphoric Monoester Hydrolases - genetics / Phosphoric Monoester Hydrolases - metabolism / Properties / Tumor proteins

2016

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2016

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2016

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Journal Article

INPP4B is an oncogenic regulator in human colon cancer

Guo, S T,

Zhang, X D,

Agoulnik, I U,

Thorne, R F,

Liu, T,

Wang, F H,

Jin, L,

Lai, F,

Zan, L K,

Yang, R H,

Farrelly, M,

Guo, X Y,

Croft, A,

Hondermarck, H,

Yan, X G,

Scott, R,

Ackland, S,

Xi, Y F,

Tseng, H-Y,

Wang, J F,

Wang, C Y,

Li, Y P,

Chi, M N,

Jiang, C C

2016

Overview

Inositol polyphosphate 4-phosphatase type II (INPP4B) negatively regulates phosphatidylinositol 3-kinase signaling and is a tumor suppressor in some types of cancers. However, we have found that it is frequently upregulated in human colon cancer cells. Here we show that silencing of INPP4B blocks activation of Akt and serum- and glucocorticoid-regulated kinase 3 (SGK3), inhibits colon cancer cell proliferation and retards colon cancer xenograft growth. Conversely, overexpression of INPP4B increases proliferation and triggers anchorage-independent growth of normal colon epithelial cells. Moreover, we demonstrate that the effect of INPP4B on Akt and SGK3 is associated with inactivation of phosphate and tensin homolog through its protein phosphatase activity and that the increase in INPP4B is due to Ets-1-mediated transcriptional upregulation in colon cancer cells. Collectively, these results suggest that INPP4B may function as an oncogenic driver in colon cancer, with potential implications for targeting INPP4B as a novel approach to treat this disease.

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Publisher

Nature Publishing Group UK,Nature Publishing Group

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13/51

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