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Tocopherol-associated protein suppresses prostate cancer cell growth by inhibition of the phosphoinositide 3-kinase pathway.

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Date
2005-11
Authors
Ni, Jing
Wen, Xingqiao
Yao, Jorge
Chang, Hong-Chiang
Yin, Yi
Zhang, Min
Xie, Shaozhen
Chen, Ming
Simons, Brenna
Chang, Philip
di Sant'Agnese, Anthony
Messing, Edward M
Yeh, Shuyuan
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Abstract
Epidemiologic studies suggested that vitamin E has a protective effect against prostate cancer. We showed here that tocopherol-associated protein (TAP), a vitamin E-binding protein, promoted vitamin E uptake and facilitated vitamin E antiproliferation effect in prostate cancer cells. Interestingly, without vitamin E treatment, overexpression of TAP in prostate cancer cells significantly suppressed cell growth; knockdown of endogenous TAP by TAP small interfering RNA (siRNA) in nonmalignant prostate HPr-1 cells increased cell growth. Further mechanism dissection studies suggested that the tumor suppressor function of TAP was via down-regulation of phosphoinositide 3-kinase (PI3K)/Akt signaling, but not by modulating cell cycle arrest or androgen receptor signaling. Immunoprecipitation results indicated that TAP inhibited the interaction of PI3K subunits, p110 with p85, and subsequently reduced Akt activity. Constitutively active Akt could negate the TAP-suppressive activity on prostate cancer cell growth. Moreover, stable transfection of TAP in LNCaP cells suppressed LNCaP tumor incidence and growth rate in nude mice. Furthermore, TAP mRNA and protein expression levels were significantly down-regulated in human prostate cancer tissue samples compared with benign prostate tissues as measured by reverse transcription-PCR, in situ hybridization, and immunohistochemistry. Together, our data suggest that TAP not only mediates vitamin E absorption to facilitate vitamin E antiproliferation effect in prostate cancer cells, but also functions like a tumor suppressor gene to control cancer cell viability through a non-vitamin E manner. Therefore, TAP may represent a new prognostic marker for prostate cancer progression.
Type
Journal article
Subject
Cell Line, Tumor
Animals
Humans
Mice
Mice, Nude
Prostatic Neoplasms
Vitamin E
Lipoproteins
Carrier Proteins
Trans-Activators
Transplantation, Heterologous
Neoplasm Transplantation
Cell Growth Processes
MAP Kinase Signaling System
Gene Expression
Male
Proto-Oncogene Proteins c-akt
Phosphatidylinositol 3-Kinases
Permalink
https://hdl.handle.net/10161/21893
Published Version (Please cite this version)
10.1158/0008-5472.can-05-1334
Publication Info
Ni, Jing; Wen, Xingqiao; Yao, Jorge; Chang, Hong-Chiang; Yin, Yi; Zhang, Min; ... Yeh, Shuyuan (2005). Tocopherol-associated protein suppresses prostate cancer cell growth by inhibition of the phosphoinositide 3-kinase pathway. Cancer research, 65(21). pp. 9807-9816. 10.1158/0008-5472.can-05-1334. Retrieved from https://hdl.handle.net/10161/21893.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Chen

Ming Chen

Assistant Professor in Pathology
Our laboratory is interested in understanding the molecular and genetic events underlying cancer progression and metastasis. The focus of our work is a series of genetically engineered mouse models that faithfully recapitulate human disease. Using a combination of mouse genetics, omics technologies, cross-species analyses and in vitro approaches, we aim to identify cancer cell–intrinsic and –extrinsic mechanisms driving metastatic cancer progression, with a long
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