Literature DB >> 14516786

Novel mechanisms of sublethal oxidant toxicity: induction of premature senescence in human fibroblasts confers tumor promoter activity.

Tarrah K Dilley1, G Tim Bowden, Qin M Chen.   

Abstract

Aging is the highest risk factor for cancer. Although oxidants are thought to contribute to both aging and cancer, the interplay between oxidative stress, aging, and cancer has not been well studied. Human diploid fibroblasts (HDFs) undergo premature senescence in response to sublethal doses of H(2)O(2). To test the hypothesis that senescent or senescent-like HDFs function as a tumor promoter, we have employed an in vitro skin tumor promotion model, in which colony formation is measured using initiated mouse keratinocyte 308 cells seeded at clonal density. 308 cells form colonies when co-cultured with normal HDFs only in the presence of the tumor promoter phorbol 12-myristate 13-acetate (TPA), which induces an average of 5.75 colonies. When co-cultured with H(2)O(2)-treated HDFs, 308 cells form an average of 30.3 colonies. To understand the mechanism behind this phenomenon, we tested whether conditioned medium of HDFs, HDF extracellular matrix (ECM), density of HDFs, or the contact between keratinocytes and HDFs plays a role in 308 cell colony formation. The conditioned medium from prematurely senescent cells resulted in an average of eightfold more 308 cell colonies formed than the conditioned medium from normal HDFs, and the growth-promoting effect of the conditioned medium was trypsin sensitive. The ECM alone was not able to induce 308 cell colony formation. Increasing the density of normal HDFs or contact with normal HDFs but not senescent-like HDFs was inhibitory to the growth of 308 cells. Measurement of Connexin 43 indicated a decreased expression of the protein, which suggests an impaired gap junction communication in senescent-like HDFs. We conclude that H(2)O(2)-treated fibroblasts not only lose contact inhibition of the growth of initiated keratinocytes perhaps related to reduced gap junction communication but also increase production of secreted protein factors to enhance the growth of 308 keratinocytes.

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Year:  2003        PMID: 14516786     DOI: 10.1016/s0014-4827(03)00308-2

Source DB:  PubMed          Journal:  Exp Cell Res        ISSN: 0014-4827            Impact factor:   3.905


  21 in total

Review 1.  The essence of senescence.

Authors:  Thomas Kuilman; Chrysiis Michaloglou; Wolter J Mooi; Daniel S Peeper
Journal:  Genes Dev       Date:  2010-11-15       Impact factor: 11.361

2.  Tiam1-regulated osteopontin in senescent fibroblasts contributes to the migration and invasion of associated epithelial cells.

Authors:  Jiewei Liu; Kun Xu; Maya Chase; Yuxin Ji; Jennifer K Logan; Rachel J Buchsbaum
Journal:  J Cell Sci       Date:  2012-02-02       Impact factor: 5.285

Review 3.  Oncogene-induced senescence and its role in tumor suppression.

Authors:  Jay P Reddy; Yi Li
Journal:  J Mammary Gland Biol Neoplasia       Date:  2011-06-18       Impact factor: 2.673

4.  Senescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimuli.

Authors:  L A Maciel-Barón; S L Morales-Rosales; A A Aquino-Cruz; F Triana-Martínez; S Galván-Arzate; A Luna-López; V Y González-Puertos; N E López-Díazguerrero; C Torres; Mina Königsberg
Journal:  Age (Dordr)       Date:  2016-02-11

Review 5.  Cellular senescence: a link between cancer and age-related degenerative disease?

Authors:  Judith Campisi; Julie K Andersen; Pankaj Kapahi; Simon Melov
Journal:  Semin Cancer Biol       Date:  2011-09-10       Impact factor: 15.707

6.  A new paradigm for the role of aging in the development of skin cancer.

Authors:  Davina A Lewis; Jeffrey B Travers; Dan F Spandau
Journal:  J Invest Dermatol       Date:  2008-09-25       Impact factor: 8.551

Review 7.  Inflammatory signaling and cellular senescence.

Authors:  Jian-Lin Ren; Jin-Shui Pan; Ya-Pi Lu; Peiqing Sun; Jiahuai Han
Journal:  Cell Signal       Date:  2008-10-26       Impact factor: 4.315

Review 8.  Senescent cells as a source of inflammatory factors for tumor progression.

Authors:  Albert R Davalos; Jean-Philippe Coppe; Judith Campisi; Pierre-Yves Desprez
Journal:  Cancer Metastasis Rev       Date:  2010-06       Impact factor: 9.264

9.  The effects of aging on the molecular and cellular composition of the prostate microenvironment.

Authors:  Daniella Bianchi-Frias; Funda Vakar-Lopez; Ilsa M Coleman; Stephen R Plymate; May J Reed; Peter S Nelson
Journal:  PLoS One       Date:  2010-09-01       Impact factor: 3.240

10.  Caveolin-1 regulates the antagonistic pleiotropic properties of cellular senescence through a novel Mdm2/p53-mediated pathway.

Authors:  Janine N Bartholomew; Daniela Volonte; Ferruccio Galbiati
Journal:  Cancer Res       Date:  2009-03-24       Impact factor: 12.701

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