Literature DB >> 7829267

Catechol interferes with TGF-beta-induced elimination of transformed cells by normal cells: implications for the survival of transformed cells during carcinogenesis.

D Schaefer1, J M Jürgensmeier, G Bauer.   

Abstract

We have recently shown that TGF-beta-treated normal fibroblasts are able to induce apoptosis of transformed fibroblasts, leading to their elimination. Here we describe a test system that allows the quantitative analysis of the elimination of G418-resistant transformed cells by TGF-beta-treated normal cells. This assay system was used to screen for substances that interfere with the elimination of transformed cells. Catechol and hydroquinone, but not resorcinol, were found to represent potent antagonists of TGF-beta-induced elimination of transformed cells by normal cells. Protection of transformed cells from negative effects derived from their cellular environment defines a hitherto unrecognized crucial mechanism for the survival of transformed cells. The protective effect of catechol as seen in this experimental system may act in concert with its co-carcinogenic and promoting activities during carcinogenesis.

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Year:  1995        PMID: 7829267     DOI: 10.1002/ijc.2910600416

Source DB:  PubMed          Journal:  Int J Cancer        ISSN: 0020-7136            Impact factor:   7.396


  4 in total

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2.  Singlet oxygen treatment of tumor cells triggers extracellular singlet oxygen generation, catalase inactivation and reactivation of intercellular apoptosis-inducing signaling.

Authors:  Michaela Riethmüller; Nils Burger; Georg Bauer
Journal:  Redox Biol       Date:  2015-07-17       Impact factor: 11.799

3.  Antiplatelet effect of catechol is related to inhibition of cyclooxygenase, reactive oxygen species, ERK/p38 signaling and thromboxane A2 production.

Authors:  Mei-Chi Chang; Hsiao-Hua Chang; Tong-Mei Wang; Chiu-Po Chan; Bor-Ru Lin; Sin-Yuet Yeung; Chien-Yang Yeh; Ru-Hsiu Cheng; Jiiang-Huei Jeng
Journal:  PLoS One       Date:  2014-08-14       Impact factor: 3.240

4.  Increasing the endogenous NO level causes catalase inactivation and reactivation of intercellular apoptosis signaling specifically in tumor cells.

Authors:  Georg Bauer
Journal:  Redox Biol       Date:  2015-08-24       Impact factor: 11.799

  4 in total

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