Stromal-epithelial interactions in aging and cancer: senescent fibroblasts alter epithelial cell differentiation

By S. Parrinello, Jean-Philippe Coppé, A. Krtolica, J. Campisi. Journal of Cell Science, 2004

622 citations recorded by the source corpus.

Subfields: Genetics, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/0aac10040c78d593b773bd5c5498b53e19de3ba0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. J. Campisi
2. Adam Freund
3. J. Kirkland
4. Jesús Gil
5. T. Rando
6. Jan H. J. Hoeijmakers
7. D. Peeper

In Oncology

1. J. Campisi
2. Jesús Gil
3. J. Kirkland
4. D. Baker
5. Bennett G. Childs
6. Adam Freund
7. F. Rodier
8. S. Khosla

In Physiology

1. J. Campisi
2. Jesús Gil
3. M. Demaria
4. J. Kirkland
5. Adam Freund
6. T. Tchkonia
7. P. Desprez
8. F. Rodier

Citations in the corpus

• p38MAPK is a novel DNA damage response‐independent regulator of the senescence‐associated secretory phenotype (2011, background): “Among the deleterious effects, SASP MMPs can disrupt mammary morphogenesis in cell culture models (Parrinello et al, 2005).”
• Inflammatory Networks during Cellular Senescence: Causes and Consequences (2010, background): “Senescent cells can disrupt normal tissue structure and function in mammary gland culture models [15], accelerate the invasion of transformed cells in a Boyden chamber assay via an epithelial to mesenchymal transition [23], stimulate both endothelial cell invasion in a Boyden chamber assay and angio”
• The essence of senescence. (2010, background): “In certain settings, pro-oncogenic effects result: The proliferative rate, migration, and invasion of premalignant cells are enhanced when they are cocultured with, or grown in medium conditioned by, senescent fibroblasts (Krtolica et al. 2001; Dilley et al. 2003; Parrinello et al. 2005; Yang et al.”
• Aging, Cellular Senescence, and Cancer (2012, background): “However, the SASP also includes proteins that have complex effects on cells—for example, the biphasic WNT modulator SFRP1 (secreted frizzled related protein 1) (98) and interleukins IL-6 and IL-8 (32, 99, 100), which can stimulate or inhibit WNT signaling and cell proliferation, respectively, depend”
• Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “3.2 Secreted proteases Aside from soluble signaling cytokines and growth factors, senescent cells also secrete increased levels of some matrix metalloproteinases (MMPs).”
• Cellular senescence and its effector programs (2014, background): “For example, these paracrine effects include promotion of epithelial–mesenchyme transition and invasion, tumor vascularization, and abnormal tissue morphology, which are mediated by the proinflammatory cytokines IL6 and IL8, VEGF, and the metalloprotease MMP3 (Parrinello et al. 2005; Coppé et al. 2”
• Senescence is a developmental mechanism that contributes to embryonic growth and patterning. (2013, background): “In some instances, the SASP can induce proliferation or epithelial-tomesenchymal transformation (EMT) and invasion in neighboring cells, exerting protumorigenic influence (Krtolica et al., 2001; Parrinello et al., 2005).”
• Senescence and apoptosis: dueling or complementary cell fates? (2014, positive): “Various components of the SASP, however, promote pre-malignant cell growth or invasion through their ability to induce angiogenesis, epithelial – mesenchymal transitions and differentiation within the local microenvironment [25,29,125 – 127].”
• Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. (2005, background): “…of cells that harbor preneoplastic mu- r tations (Figure 2B). s Recent findings suggest that senescent fibroblasts r can disrupt the functional and morphological differenti- t ation of epithelial cells, at least in three-dimensional cultures of mammary epithelial cells (Parrinello et al., 2005).”
• Chemokine signaling via the CXCR2 receptor reinforces senescence. (2008, background): “For example, senescent fibroblasts can stimulate angiogenesis (Coppe et al., 2006), alter differentiation (Parrinello et al., 2005), and promote growth and tumorigenesis of epithelial cells (Krtolica et al., 2001).”
• Lamin B1 loss is a senescence-associated biomarker (2012, background): “They have also been shown to accumulate at sites of age-related pathology, both degenerative and preneoplastic (Parrinello et al., 2005; Campisi and d’Adda di Fagagna, 2007; Jeyapalan and Sedivy, 2008; Collado and Serrano, 2010).”
• Fat Tissue, Aging, and Cellular Senescence (2010, background): “Cellular senescence leads to a senescent secretory phenotype with increased inflammatory cytokines, altered production of ECM-modifying proteases, and production of ROS (Freund et al.; Passos et al. 2010; Krtolica & Campisi, 2002; Parrinello et al., 2005; Xue et al., 2007; Coppé et al., 2008).”
• An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA. (2026, background): “Senescent cells accumulate with age and are thought to contribute to age-related diseases through the SASP (Coppé et al., 2008, 2010a; Krtolica et al., 2001; Parrinello et al., 2005).”
• Persistent DNA damage signaling triggers senescence-associated inflammatory cytokine secretion (2009, neutral): “The SASP can disrupt normal mammary differentiatio”
• Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor (2008, neutral): “hyperproliferative changes in neighboring cells [35,39,42,43].”