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Characteristics, Events, and Stages in Tumorigenesis
Published in Franklyn De Silva, Jane Alcorn, The Elusive Road Towards Effective Cancer Prevention and Treatment, 2023
Franklyn De Silva, Jane Alcorn
Traditionally, cancer treatment was based on the idea that almost all somatic cells have similar malignant potential [117]. However, tumor tissue is supported by a few dedicated stem cells within the tumor environment [817]. Those cells containing stem cell-like characteristics can give rise to cancers and become a source of cells that give rise to distant metastases [818]. Targeted drugs that cause the regression of primary tumors often fail to eliminate CSCs, placing patients at risk of recurrence, particularly after discontinuation of drug administration [117]. Cancer stem cells can support self-renewal cloning, metastasis, growth, homing, and reproliferation of tumors [819], and give rise to heterogeneous cell populations with high plasticity potential [820, 821], resistance to stressful factors such as low nutrient or oxygen levels, resistance to apoptosis [761, 822], enhanced accumulation of mutations [819], and quiescence [819, 823, 824]. Furthermore, the collective evidence suggests that progenitor cell pools within tumors revert to cancer stem cells through mechanisms such as EMT [819, 825, 826]. EMT is a vital procedure through which nearly all mature tissues sustain their migratory competence in normal embryogenesis, wound healing, and tissue repair [827]. The occurrence of ‘partial EMT' has also been reported in favoring progression and metastasis of cancer [281]. In general, CSCs and undetectable micrometastases continue to be a major challenge in breast and prostate cancer patients and complicate the planning of effective treatment options.
Implantation and In Utero Growth
Published in Arianna D'Angelo, Nazar N. Amso, Ultrasound in Assisted Reproduction and Early Pregnancy, 2020
Kugajeevan Vigneswaran, Ippokratis Sarris
Despite the evidence collated in the literature, the issue of EMT remains unresolved. A recent study in 2015 that only looked at euploid embryos being implanted concluded that EMT has no impact on implantation and that the morphology of the endometrium on the day of trigger for final oocyte maturation may be more of a sensitive marker of successful outcomes [4].
Indian Diet and Cancer Prevention
Published in Sheeba Varghese Gupta, Yashwant V. Pathak, Advances in Nutraceutical Applications in Cancer, 2019
Vasudha Pritipaul, Asra Sami, Sheeba Varghese Gupta
Thymoquinone can also impact epithelial to mesenchymal transition (EMT) of cervical cancer cells. EMT is thought to encourage cancer metastasis, and thymoquinone limited the effect of the transcription factors that contribute to EMT [63].
Epithelial cell dysfunction in chronic rhinosinusitis: the epithelial–mesenchymal transition
Published in Expert Review of Clinical Immunology, 2023
Jing Yuan, Ming Wang, Chengshuo Wang, Luo Zhang
EMT is accompanied by a decrease in epithelial cell markers and an increase in mesenchymal cell markers. TGF-β signaling pathway, hypoxia and HIF-α-related pathway, Wnt/β-catenin signaling, and MAPK pathway have been shown to be closely associated with the EMT process. These signaling pathways function independently or collectively to promote EMT, and thus involve complex underlying mechanisms. Blocking the signaling molecules related to these pathways thus provides an opportunity to inhibit EMT. In this regard, TGF-β and its downstream signals have been widely explored as potential targets for the inhibition and/or reversal of EMT. While research into other signaling pathways is currently limited. To treat CRS in the future, personalized therapy strategies are required because the current mechanisms of EMT are still controversial and inconsistent in CRSsNP and CRSwNP.
Cyclophilin A/CD147 signaling induces the epithelial-to-mesenchymal transition and renal fibrosis in chronic allograft dysfunction by regulating p38 MAPK signaling
Published in Renal Failure, 2022
Xuzhong Liu, Zhiwang Tang, Xi Jiang, Tianwei Wang, Lun Zhao, Zongyuan Xu, Kun Liu
Epithelial-to-mesenchymal transition (EMT), characterized as the loss of epithelial cell markers (E-cadherin) and subsequently acquired the ability of mesenchymal markers [vimentin, α-smooth muscle actin (α-SMA)], has been extensively explored in the wound healing, cancer metastasis, and organ fibrosis in past decades [6]. A large number of studies have suggested the possibility of EMT in renal fibrosis in vivo and vitro, and particularly, in allograft interstitial fibrosis through classical and non-classical pathways [3,7]. The supportive evidence of EMT in renal fibrosis have been provided in a variety of basic studies using different animal models and genetic lineage tracing systems, suggesting that EMT is partially responsible for the occurrence and development of renal fibrosis [8–10]. Nevertheless, the therapeutic target and molecular mechanism involved in EMT requires further investigation.
MMP-3 activation is involved in copper oxide nanoparticle-induced epithelial-mesenchymal transition in human lung epithelial cells
Published in Nanotoxicology, 2021
Yuanbao Zhang, Yiqun Mo, Jiali Yuan, Yue Zhang, Luke Mo, Qunwei Zhang
Epithelial-mesenchymal transition (EMT) is a cellular process, characterized by loss of cell polarity and cell-cell adhesion, and gain of mesenchymal cell properties, which is crucial for organ development, wound healing, as well as development of diseases, such as fibrosis and cancer (Sciacovelli and Frezza 2017; Thiery et al. 2009; Willis, duBois, and Borok 2006). During EMT, expression of epithelial markers such as E-cadherin and other cell junction proteins are lost or decreased, whereas expression of mesenchymal markers such as vimentin, α-smooth muscle actin (α-SMA), and fibronectin are increased. Many factors can trigger EMT process including TGF-1, PDGF, chemokines, and MMPs. MMP-3 has been reported to promote EMT (Radisky et al. 2005; Yamashita et al. 2011). Nanoparticles can activate EMT and further contribute to nanoparticle-induced lung inflammation and fibrosis (Chang et al. 2012; Ma et al. 2017; Setyawati et al. 2018). However, few studies investigated the role of MMP-3 in metal nanoparticle-induced EMT and lung fibrosis. Therefore, to explore the relationship between MMP-3 and EMT after metal nanoparticle exposure will help us fully understand the mechanisms of metal nanoparticle-induced various toxic effects including pulmonary fibrosis.