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We began analyzing https://link.springer.com/article/10.1007/s12307-011-0069-4, but it redirected us to https://link.springer.com/article/10.1007/s12307-011-0069-4. The analysis below is for the second page.

Title[redir]:
Epithelial-Mesenchymal Transition Induced by Senescent Fibroblasts | Cancer Microenvironment
Description:
Depending on the cell type and tissue environment, epithelial and mesenchymal cell phenotypes are not static and can be highly dynamic. Epithelial-mesenchymal transitions (EMTs) and reverse EMTs provide flexibility during embryogenesis. While EMTs are a critical normal process during development and wound healing, properties of the EMT have been implicated in human pathology, particularly cancer metastasis. A normal undamaged epithelium does not typically exhibit features of an EMT. However, particularly under the influence of the surrounding microenvironment, cancer cells may reactivate developmental phenotypes out of context in the adult. This reactivation, such as the EMT, can facilitate tumor cell invasion and metastasis, and therefore is a major mechanism of tumor progression. Conversely, cellular senescence, which is associated with aging, is a process by which cells enter a state of permanent cell cycle arrest, thereby constituting a potent tumor suppressive mechanism. However, accumulating evidence shows that senescent cells can have deleterious effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescence-associated secretory phenotype (SASP) that turns senescent fibroblasts into pro-inflammatory cells having the ability to promote tumor progression, in part by inducing an EMT in nearby epithelial cells. Here, we summarize the potential impacts of SASP factors, particularly interleukins, on tissue microenvironments and their ability to stimulate tumor progression through induction of an EMT.

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Keywords {🔍}

article, google, scholar, pubmed, cas, cancer, cell, senescence, cells, tumor, biol, fibroblasts, epithelialmesenchymal, res, transition, human, senescent, cellular, microenvironment, progression, aging, growth, access, breast, nature, rev, epithelial, emt, metastasis, nat, privacy, cookies, content, research, campisi, tissue, senescenceassociated, mol, coppe, usa, publish, search, june, pierreyves, desprez, normal, invasion, secretory, sasp, open,

Topics {✒️}

ras-raf-mek-erk signaling pathway epithelial-mesenchymal transition induced epithelial-mesenchymal transition biomarkers month download article/chapter epithelial-mesenchymal transition mesenchymal-epithelial transition pierre-yves desprez dna damage-mediated induction nf-kappab-dependent manner epithelial-mesenchymal transitions tumor-promoting cell type mesenchymal cell phenotypes orchestrate tumor-promoting inflammation full article pdf human breast cancer—observations related subjects ets1 transcription factor oncogene-induced senescence increases migration radiation-induced increase stem cells nearby epithelial cells privacy choices/manage cookies stromal-epithelial interactions therapy-induced senescence breast tissue microenvironment primary human fibroblasts promote tumor progression article laberge tumor cell interactions reactivate developmental phenotypes mouse cells dependent turns senescent fibroblasts tumor-stromal interactions tumor suppressor maspin telomere-initiated senescence pancreatic cancer cells human intervertebral discs human life-spans cellular proliferation p53 tumor suppressor european economic area normal undamaged epithelium typically exhibit features check access adda di fagagna limiting cartilage repair bone joint surg matrix metalloproteinase inhibitor rate-limiting step

Questions {❓}

Dimri GP (2005) What has senescence got to do with cancer?
Homey B, Muller A, Zlotnik A (2002) Chemokines: agents for the immunotherapy of cancer?

Schema {🗺️}

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