Epithelial Mesenchymal Transition: a double‐edged sword

Barrière, Guislaine; Fici, Pietro; Gallerani, Giulia; Fabbri, Francesco; Rigaud, M.

doi:10.1186/s40169-015-0055-4

Cited by 129 publications

(94 citation statements)

References 83 publications

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“…Tumor-associated fibroblasts (TAFs) can be originated from mesenchymal or bone marrow stem cells [21]. TAFs were found to contribute to the inflammatory immunosuppressive milieu within tumor microenvironment, probably through the overexpression and upregulation of fibroblast activation protein-α, rapid hypoxic necrosis of tumor, activation of stromal cells, or cytotoxicity of IFNγ or TNFα-mediated CD8+ T cells [22].…”

Section: Roles Of Inflammatory Cells In Cancer-related Inflammationmentioning

confidence: 99%

Targeting roles of inflammatory microenvironment in lung cancer and metastasis

Shi

Wang

Hou

et al. 2015

Cancer Metastasis Rev

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Inflammatory cells and mediators are essential components in tumor microenvironment and play decisive roles in the initiation, proliferation, survival, promotion, invasion, or metastasis of lung cancer. Clinical and epidemiologic studies suggested a strong association between inflammation and lung cancer and an influence of immune surveillances and tumor responses to chemotherapeutic drugs, although roles of inflammation in lung cancer remain unclear. The present review outlined roles of inflammation in lung cancer, with particular focus on inflammatory components, types, biomarkers, or principal mechanisms by which the inflammation contributes to the development of lung cancer. The cancer-associated inflammatory cells (CICs) should be furthermore defined and include cancer-specific and interacted cells with inflammatory or inflammation-like characteristics, e.g., innate or adaptive immune cells and cancer tissue cells. We also discuss targeting potentials of inflammation in the prevention and treatment of lung cancer. The diversity of cancer-related inflammatory microenvironment is instrumental to design novel therapeutic approaches for lung cancer.

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Section: Roles Of Inflammatory Cells In Cancer-related Inflammationmentioning

confidence: 99%

Targeting roles of inflammatory microenvironment in lung cancer and metastasis

Shi

Wang

Hou

et al. 2015

Cancer Metastasis Rev

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“…beta-catenin within the context of TCF/WNT signals, Notch, Hedgehog and BMP), (iii) anaerobic metabolism. Moreover, the epithelial-mesenchymal transition (EMT), a normal cellular process that regulates embryogenesis and wound healing, is exploited during tumor progression to generate a metastatic cellular phenotype and can also be viewed as a reactivation of an embryonic program [98][99][100].…”

Section: Cancer Stem Cell Reprogrammingmentioning

confidence: 99%

Cancer Stem Cells: Foe or Reprogrammable Cells for Efficient Cancer Therapy?

Ventura¹,

Olivi²,

Cavallini³

et al. 2015

NanoWorld J

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Embryonic development and carcinogenesis share many molecular pathways and regulatory molecules. While the induction of a pluripotent state involves a significant oncogenic risk, as in induced pluripotent stem cells (iPSCs), the embryonic environment in vivo has been shown to suppress tumor development. In this review, we discuss the subtle equilibrium between the nanotopography (niche) of the hosting tissue resident stem cells and their biological dynamics, including the transformation in cancer stem cells. We review consistent findings indicating the potential for modulating the biology of human cancer stem cells by the aid of naturally occurring or synthetic molecules, including developmental stage zebrafish embryo extracts, hyaluronan, butyric acid (BA) and retinoic acid (RA), hyaluronan mixed esters of BA and RA, melatonin, vitamin D3, and endorphin peptides. Within this context, we dissect the multifaceted mechanisms orchestrated by endorphinergic systems, including paracrine cellto-cell communication, as well as the establishment of autocrine and intracrine (intracellular) peptide actions driving transcriptional responses and self-sustaining loops that behave as long-lived signals imparting features characteristic of differentiation, growth regulation and cell memory.Based upon the remarkable action of electromagnetic fields and mechanical vibration on (stem) cell signaling, differentiation, and senescence, we also consider the potential for using these physical energies as a tool to afford a fine tuning of cancer stem cell fate.On the whole, we forecast future deployment of the physical and/or chemical approaches described herein aiming at reprogramming, rather than destroying cancer stem cells, eventually placing cancer therapy within the context of Regenerative Medicine.

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“…40 In the context of wound healing, EMT is driven by cytokines such as TGF-b and is necessary for sedentary proliferative keratinocytes to migrate toward the center of the wound. In normal wound healing, this process leads to reepithelialization; however, excess migration may lead to fibrosis and hypertrophic scarring.…”

Section: Mirnas Regulate Epithelialmesenchymal Transitionmentioning

confidence: 99%