TGFβ1 induces caspase-dependent but death-receptor independent apoptosis in lymphoid cells

A. Tótth, A. Sebestyén, G. Barna, K. Nagy, A. Göndör, J. Bocsi, R. Mihalik, I. Peták, J. Houghton, L. Kopper

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Transforming growth factor beta 1 (TGFβ1) is an antiproliferative and proapoptotic cytokine for normal B-cells, however many B-cell lymphomas have lost their response to TGFβ1. The aim of this study was to identify the sequence of events in apoptosis induced by TGFβ1 in an EBV negative, human B-cell lymphoma line (HT58). The proportion of apoptotic cells increased gradually (up to 72 hr) at an optimal dose range of 0.5-1.0 ng/ml. The induced cell death required the action of downstream caspases. Caspase activation was accompanied by an increase in the permeability of mitochondrial membranes, but there was no change in the expression of certain members of Bcl-2 family (Bcl-2, Bax, Bcl-XL). Similarly, none of the death receptors or ligands were involved in apoptosis induction. Further study will include the participation of TGFβ1 target genes in the pore formation of mitochondrial membranes and/or the elimination ora putative survival signal.

Original languageEnglish
Pages (from-to)1207-1212
Number of pages6
JournalAnticancer research
Volume21
Issue number2 A
Publication statusPublished - Jun 11 2001

Keywords

  • Apoptosis
  • Caspases
  • Death receptors
  • Lymphoma
  • Mitochondria
  • TGFβ1

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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