TGFβ1 kills lymphoma cells using mitochondrial apoptotic pathway with the help of caspase-8

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14 Citations (Scopus)

Abstract

It is a known paradox that many TGFβ1-producing tumor cells are resistant to this, otherwise, inhibitory cytokine. In a lymphoma of B-cell origin exogenous TGFβ1 was able to induce apoptosis, suggesting that the apoptosis program can be switched on. The apoptosis induction was independent of the death receptors but dependent on mitochondrial pathway and caspase-3. Probably due to the weak starting signal, caspase-3 further activated caspase-8 which, through the Bid cleavage and Bax translocation into the mitochondria, provided an autocatalytic support for the apoptotic program. There is a time-gap between the early activation of Smad-dependent TIEG and the accumulation of ROS, therefore other participants that start the increase in mitochondrial membrane permeability should be identified.

Original languageEnglish
Pages (from-to)3867-3872
Number of pages6
JournalAnticancer Research
Volume22
Issue number6 C
Publication statusPublished - Nov 2002

Fingerprint

Caspase 8
Lymphoma
Apoptosis
Caspase 3
Death Domain Receptors
Mitochondrial Membranes
B-Cell Lymphoma
Permeability
Mitochondria
Cytokines
Neoplasms

Keywords

  • Apoptosis
  • Bax
  • Bid
  • Caspase-8
  • Lymphoma
  • TGFβ1
  • TIEG

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

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title = "TGFβ1 kills lymphoma cells using mitochondrial apoptotic pathway with the help of caspase-8",
abstract = "It is a known paradox that many TGFβ1-producing tumor cells are resistant to this, otherwise, inhibitory cytokine. In a lymphoma of B-cell origin exogenous TGFβ1 was able to induce apoptosis, suggesting that the apoptosis program can be switched on. The apoptosis induction was independent of the death receptors but dependent on mitochondrial pathway and caspase-3. Probably due to the weak starting signal, caspase-3 further activated caspase-8 which, through the Bid cleavage and Bax translocation into the mitochondria, provided an autocatalytic support for the apoptotic program. There is a time-gap between the early activation of Smad-dependent TIEG and the accumulation of ROS, therefore other participants that start the increase in mitochondrial membrane permeability should be identified.",
keywords = "Apoptosis, Bax, Bid, Caspase-8, Lymphoma, TGFβ1, TIEG",
author = "G. Barna and A. Sebesty{\'e}n and C. Chinopoulos and Katalin Nagy and R. Mihalik and S. Paku and L. K{\'o}pper",
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T1 - TGFβ1 kills lymphoma cells using mitochondrial apoptotic pathway with the help of caspase-8

AU - Barna, G.

AU - Sebestyén, A.

AU - Chinopoulos, C.

AU - Nagy, Katalin

AU - Mihalik, R.

AU - Paku, S.

AU - Kópper, L.

PY - 2002/11

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N2 - It is a known paradox that many TGFβ1-producing tumor cells are resistant to this, otherwise, inhibitory cytokine. In a lymphoma of B-cell origin exogenous TGFβ1 was able to induce apoptosis, suggesting that the apoptosis program can be switched on. The apoptosis induction was independent of the death receptors but dependent on mitochondrial pathway and caspase-3. Probably due to the weak starting signal, caspase-3 further activated caspase-8 which, through the Bid cleavage and Bax translocation into the mitochondria, provided an autocatalytic support for the apoptotic program. There is a time-gap between the early activation of Smad-dependent TIEG and the accumulation of ROS, therefore other participants that start the increase in mitochondrial membrane permeability should be identified.

AB - It is a known paradox that many TGFβ1-producing tumor cells are resistant to this, otherwise, inhibitory cytokine. In a lymphoma of B-cell origin exogenous TGFβ1 was able to induce apoptosis, suggesting that the apoptosis program can be switched on. The apoptosis induction was independent of the death receptors but dependent on mitochondrial pathway and caspase-3. Probably due to the weak starting signal, caspase-3 further activated caspase-8 which, through the Bid cleavage and Bax translocation into the mitochondria, provided an autocatalytic support for the apoptotic program. There is a time-gap between the early activation of Smad-dependent TIEG and the accumulation of ROS, therefore other participants that start the increase in mitochondrial membrane permeability should be identified.

KW - Apoptosis

KW - Bax

KW - Bid

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KW - Lymphoma

KW - TGFβ1

KW - TIEG

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