Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells.

Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells. Research Abstract Details 

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Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells. Abstract Text:

Junyang Gong,JuneGoo Lee,Horiguchi Akio,Peter N Schlegel,Ruoqian Shen,

Multiple studies indicate that neuroendocrine (NE) differentiation in prostate cancer (PC) contributes to androgen-independent progression. Levels of chromogranin A (CgA), which is produced by NE cells, are increased in advanced PC. However, the mechanism by which high levels of circulating CgA contribute to PC progression is unknown. To examine the effects of CgA on PC cells, we first performed proliferation assays in the presence of recombinant CgA (rCgA) in LNCaP and C4-2 PC cells, and found that rCgA increased cell proliferation in a dose and time-dependent manner. NE differentiated PC cells, also overexpress the antiapoptosis protein survivin. Therefore, we examined survivin expression in the presence of CgA in PC cells. Western blot analysis showed that survivin was significantly increased by rCgA and inhibited by an anti-CgA antibody in both LNCaP and C4-2 cells. Survivin expression is believed to be regulated by PI3K/Akt pathway. We next assessed the phosphorylation status of Akt and found that Akt phosphorylation was increased by treatment with rCgA. To determine whether Akt phosphorylation is necessary for rCgA-induced survivin expression, we examined the effects of Akt, MAPK kinase, and protein kinase C inhibitors on CgA-induced survivin expression, and found that survivin expression was reduced in the presence of Akt inhibitors, but not MAPK kinase or protein kinase C inhibitors. Furthermore, in the presence of an Akt inhibitor or small interfering RNA of survivin, CgA-enhanced proliferation of C4-2 and LNCaP cells significantly decreased. Together, our results demonstrate that CgA can increase PC cell survival through Akt-mediated survivin up-regulation.

Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells. Publishing Authors By Initials

J Gong,J Lee,H Akio,PN Schlegel,R Shen,

For similar genetic processes: gene expression regulation: up-regulation research abstracts see: genetic processes: gene expression regulation: up-regulation research

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Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Endocrinology

VOLUME: 148

Page Numbers: 4489-99

Journal Abbreviation: Endocrinology

ISSN: 0013-7227

DAY: 21

MONTH: 06

YEAR: 2007

Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 375040

Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells. Keywords Mesh Terms:

KEYWORDS: Up-Regulation

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells. Information

Substance Name: Proto-Oncogene Proteins c-akt

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells.

AFFILIATION: Weill Medical College of Cornell University, Department of Urology, Room E-300, Box 23, 1300 York Avenue, New York, New York 10021, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: R01 DK060908-02

ACRONYM: DK

MEDLINETA: Endocrinology

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