Programmed cell death 6 (PDCD6) inhibits angiogenesis through PI3K/mTOR/p70S6K pathway by interacting of VEGFR-2

Seung Bae Rho, Yong Jung Song, Myong Cheol Lim, Seung Hoon Lee, Boh Ram Kim, Sang Yoon Park

Research output: Contribution to journalArticleResearchpeer-review

39 Citations (Scopus)

Abstract

Programmed cell death 6 (PDCD6) was originally found as a pro-apoptotic protein, but its molecular mechanism is not well understood. In this study, we have attempted to investigate the effects of PDCD6 on the inhibition of angiogenesis-mediated cell growth as a novel anti-angiogenic protein. Purified recombinant human PDCD6 inhibited cell migration in a concentration-time-dependent manner. We also found that overexpressed PDCD6 suppressed vascular endothelial growth factor (VEGF)-induced proliferation, invasion, and capillary-like structure tube formation in vitro. PDCD6 suppressed phosphorylation of signaling regulators downstream from PI3K, including Akt, mammalian target of rapamycin (mTOR), glycogen synthase kinase-3β(GSK-3β), ribosomal protein S6 kinase (p70S6K), and also decreased cyclin D1 expression. We found binding PDCD6 to VEGFR-2, a key player in the PI3K/mTOR/P70S6K signaling pathway. Taken together, these data suggest that PDCD6 plays a significant role in modulating cellular angiogenesis.

Original languageEnglish
Pages (from-to)131-139
Number of pages9
JournalCellular Signalling
Volume24
Issue number1
DOIs
StatePublished - 1 Jan 2012

Fingerprint

70-kDa Ribosomal Protein S6 Kinases
Vascular Endothelial Growth Factor Receptor-2
Sirolimus
Phosphatidylinositol 3-Kinases
Cell Death
Angiogenic Proteins
Ribosomal Protein S6 Kinases
Glycogen Synthase Kinase 3
Apoptosis Regulatory Proteins
Cyclin D1
Vascular Endothelial Growth Factor A
Cell Movement
Phosphorylation
Growth

Keywords

  • Angiogenesis
  • Apoptosis
  • Endothelial cell
  • PI3K/mTOR/p70S6K pathway
  • Programmed cell death 6

Cite this

Rho, Seung Bae ; Song, Yong Jung ; Lim, Myong Cheol ; Lee, Seung Hoon ; Kim, Boh Ram ; Park, Sang Yoon. / Programmed cell death 6 (PDCD6) inhibits angiogenesis through PI3K/mTOR/p70S6K pathway by interacting of VEGFR-2. In: Cellular Signalling. 2012 ; Vol. 24, No. 1. pp. 131-139.
@article{8a9f567e6038413c8d2b02037d6050d9,
title = "Programmed cell death 6 (PDCD6) inhibits angiogenesis through PI3K/mTOR/p70S6K pathway by interacting of VEGFR-2",
abstract = "Programmed cell death 6 (PDCD6) was originally found as a pro-apoptotic protein, but its molecular mechanism is not well understood. In this study, we have attempted to investigate the effects of PDCD6 on the inhibition of angiogenesis-mediated cell growth as a novel anti-angiogenic protein. Purified recombinant human PDCD6 inhibited cell migration in a concentration-time-dependent manner. We also found that overexpressed PDCD6 suppressed vascular endothelial growth factor (VEGF)-induced proliferation, invasion, and capillary-like structure tube formation in vitro. PDCD6 suppressed phosphorylation of signaling regulators downstream from PI3K, including Akt, mammalian target of rapamycin (mTOR), glycogen synthase kinase-3β(GSK-3β), ribosomal protein S6 kinase (p70S6K), and also decreased cyclin D1 expression. We found binding PDCD6 to VEGFR-2, a key player in the PI3K/mTOR/P70S6K signaling pathway. Taken together, these data suggest that PDCD6 plays a significant role in modulating cellular angiogenesis.",
keywords = "Angiogenesis, Apoptosis, Endothelial cell, PI3K/mTOR/p70S6K pathway, Programmed cell death 6",
author = "Rho, {Seung Bae} and Song, {Yong Jung} and Lim, {Myong Cheol} and Lee, {Seung Hoon} and Kim, {Boh Ram} and Park, {Sang Yoon}",
year = "2012",
month = "1",
day = "1",
doi = "10.1016/j.cellsig.2011.08.013",
language = "English",
volume = "24",
pages = "131--139",
journal = "Cellular Signalling",
issn = "0898-6568",
publisher = "Elsevier Inc.",
number = "1",

}

Programmed cell death 6 (PDCD6) inhibits angiogenesis through PI3K/mTOR/p70S6K pathway by interacting of VEGFR-2. / Rho, Seung Bae; Song, Yong Jung; Lim, Myong Cheol; Lee, Seung Hoon; Kim, Boh Ram; Park, Sang Yoon.

In: Cellular Signalling, Vol. 24, No. 1, 01.01.2012, p. 131-139.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Programmed cell death 6 (PDCD6) inhibits angiogenesis through PI3K/mTOR/p70S6K pathway by interacting of VEGFR-2

AU - Rho, Seung Bae

AU - Song, Yong Jung

AU - Lim, Myong Cheol

AU - Lee, Seung Hoon

AU - Kim, Boh Ram

AU - Park, Sang Yoon

PY - 2012/1/1

Y1 - 2012/1/1

N2 - Programmed cell death 6 (PDCD6) was originally found as a pro-apoptotic protein, but its molecular mechanism is not well understood. In this study, we have attempted to investigate the effects of PDCD6 on the inhibition of angiogenesis-mediated cell growth as a novel anti-angiogenic protein. Purified recombinant human PDCD6 inhibited cell migration in a concentration-time-dependent manner. We also found that overexpressed PDCD6 suppressed vascular endothelial growth factor (VEGF)-induced proliferation, invasion, and capillary-like structure tube formation in vitro. PDCD6 suppressed phosphorylation of signaling regulators downstream from PI3K, including Akt, mammalian target of rapamycin (mTOR), glycogen synthase kinase-3β(GSK-3β), ribosomal protein S6 kinase (p70S6K), and also decreased cyclin D1 expression. We found binding PDCD6 to VEGFR-2, a key player in the PI3K/mTOR/P70S6K signaling pathway. Taken together, these data suggest that PDCD6 plays a significant role in modulating cellular angiogenesis.

AB - Programmed cell death 6 (PDCD6) was originally found as a pro-apoptotic protein, but its molecular mechanism is not well understood. In this study, we have attempted to investigate the effects of PDCD6 on the inhibition of angiogenesis-mediated cell growth as a novel anti-angiogenic protein. Purified recombinant human PDCD6 inhibited cell migration in a concentration-time-dependent manner. We also found that overexpressed PDCD6 suppressed vascular endothelial growth factor (VEGF)-induced proliferation, invasion, and capillary-like structure tube formation in vitro. PDCD6 suppressed phosphorylation of signaling regulators downstream from PI3K, including Akt, mammalian target of rapamycin (mTOR), glycogen synthase kinase-3β(GSK-3β), ribosomal protein S6 kinase (p70S6K), and also decreased cyclin D1 expression. We found binding PDCD6 to VEGFR-2, a key player in the PI3K/mTOR/P70S6K signaling pathway. Taken together, these data suggest that PDCD6 plays a significant role in modulating cellular angiogenesis.

KW - Angiogenesis

KW - Apoptosis

KW - Endothelial cell

KW - PI3K/mTOR/p70S6K pathway

KW - Programmed cell death 6

UR - http://www.scopus.com/inward/record.url?scp=80755175776&partnerID=8YFLogxK

U2 - 10.1016/j.cellsig.2011.08.013

DO - 10.1016/j.cellsig.2011.08.013

M3 - Article

VL - 24

SP - 131

EP - 139

JO - Cellular Signalling

JF - Cellular Signalling

SN - 0898-6568

IS - 1

ER -