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Small Interfering RNAs, MicroRNAs, and NPs in Gynecological Cancers
Published in Loutfy H. Madkour, Nanoparticle-Based Drug Delivery in Cancer Treatment, 2022
EMT is an important mechanism that plays a key role in invasion and metastasis of cancer cells. A number of miRNAs have been demonstrated to regulate EMT, thereby playing a role in the regulation of invasion and metastasis. miR-200 family, a known family of tumor suppressor miRNAs with well-characterized role in EMT of cancer cells [385], has been implicated in EMT of OC cells [386,387] as well as CC cells [388,389]. Another member of this family, miR-429, has also been shown to reverse EMT [390]. miR-200a’s role in suppressing OC invasion has been attributed to its ability to target CD133/1-positive OC stem cells [356], while the ability of miR-200c to inhibit metastasis has been linked to down-regulation of mesenchymal markers vimentin/ZEB1 and up-regulation of epithelial marker E-cadherin in CD117 and CD44-positive OC stem cells [357].
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Published in Chad A. Mirkin, Spherical Nucleic Acids, 2020
Tiffany L. Halo, Kaylin M. McMahon, Nicholas L. Angeloni, Yilin Xu, Wei Wang, Alyssa B. Chinen, Dmitry Malin, Elena Strekalova, Vincent L. Cryus, Chonghui Cheng, Chad A. Mirkin, Shad Thaxton
Tumor metastasis is believed to progress through a series of steps by which cancer cells originating at a primary tumor intravasate into the blood stream, travel through the blood stream, extravasate, and form secondary tumors at distal sites [2, 7]. Recent studies have indicated that metastatic tumor cells frequently hijack the developmental program of epithelial–mesenchymal transition (EMT) for dissemination to distant organs [7, 8]. At the molecular level, EMT involves the cellular loss of epithelial markers (e.g., E-cadherin, a transmembrane cell adhesion protein) and increased expression of mesenchymal markers (e.g., Vimentin, a type II intermediate filament protein; Fibronectin, an extracellular matrix binding glycoprotein) [7–10]. The loss of intercellular contacts and apical–basal polarity during EMT results in a more invasive and migratory phenotype of tumor cells. Ultimately, it is believed that cancer cells that have entered the bloodstream must also reverse the process of EMT to colonize distal organs [11].
The Multiple Facets of Mesenchymal Stem Cells in Modulating Tumor Cells’ Proliferation and Progression
Published in Jince Thomas, Sabu Thomas, Nandakumar Kalarikkal, Jiya Jose, Nanoparticles in Polymer Systems for Biomedical Applications, 2019
Rajesh Ramasamy, Vahid Hosseinpour Sarmadi
Under the influence of certain reversible biological processes and biochemical molecules, epithelial cells are able to transdifferentiate phenotypically into MSCs. These transdifferentiated cells display MSCs features, and this process is called EMT or epithelial-mesenchymal transition.61,62 Previous studies have demonstrated that MSCs secrete soluble factors such as FGF, HGF, PDGF, and TGF-β molecules which can act as EMT-inducing agents.37,40 During the EMT process, the epithelial cells lose its cell-to-cell contact and morphologically resemble MSCs.63 Although EMT is a critical process during embryonic development and wound healing64; however, an aberrant EMT could possibly induce cancer cell metastasis, invasion and increase resistance to apoptosis.65,66 In line with these findings, Mele et al. have confirmed that MSCs derived from EMT process favor the occurrence of an aggressive human colorectal cancer through TGF-β.66 Furthermore, Strong et al. showed that leptin produced by MSCs supports the breast cancer cell growth and progression which may result from increased EMT and metastasis genes (IL-6, MMP-2, and SERPINE1) expression.67 Additionally, exosomes derived from MSCs promote proliferation, tumorigenesis, and migration of nasopharyngeal carcinoma cells (NPCs) by FGF19-mediated activation of the FGFR4 signaling cascade and consequently induce EMT.68
Methanolic extract of Teucrium persicum up-regulates and induces the membrane restoration of E-cadherin protein in PC-3 cells
Published in International Journal of Environmental Health Research, 2023
Majid Tafrihi, Anahita Naeimi, Fatemeh Eizadifard
In this study, we aimed to scrutinize the effect of T. persicum methanolic extract on E-cadherin protein expression and its cellular localization. Our immunofluorescence experiments revealed the restoration of E-cadherin protein at cell adhesion contact sites in PC-3 cells treated with 10 and 25 µg/ml of T. persicum extract. Our microscopic observations showed that T. persicum methanolic extract induced an epithelial-like morphology in PC3-treated cells compared to non-treated cells. In epithelial-mesenchymal transition (EMT), loss of cell-cell adhesion and acquisition of migratory and invasive properties can occur (Lai et al. 2020). Downregulation of E-cadherin followed by the loss of tissue integrity is an important feature of EMT (Lu and Kang 2019). Therefore, EMT reversion which is called mesenchymal-epithelial transition (MET) can be an effective strategy to hit the cancer progression and metastasis. The ability of T. persicum extract to induce the membrane centralization of E-cadherin at cell-cell contact sites is a significant anticancer potential of this Iranian endemic species, which has not been reported, yet. It is consistently maintained that the β-catenin protein is a negative regulator of E-cadherin transcription (Zhao et al. 2010). Therefore, it is aligned with our previous results that membrane localization of the β-catenin protein in PC-3 treated cells treated with T. persicum extract resulted in the induction of epithelial-like phenotype and upregulation of E-cadherin protein (Barati et al. 2021).
Atmospheric fine particulate matter and epithelial mesenchymal transition in pulmonary cells: state of the art and critical review of the in vitro studies
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Margaux Cochard, Frédéric Ledoux, Yann Landkocz
Oxidative stress, inflammation and genotoxicity seem to be the first mechanisms involved in PM-mediated toxicity (Ghio, Carraway, and Madden 2012; Gualtieri et al. 2017) which are closely related to other cascading mechanisms leading to severe diseases. However, only a few studies focused on the epithelial-mesenchymal transition (EMT), which is involved in several pulmonary fibrotic diseases and lung cancer metastasis (Acloque et al. 2009; Bartis et al. 2014; Kalluri and Weinberg 2009; Thiery 2002; Thiery et al. 2009). EMT is a biological process based upon epithelial cells modulation into mesenchymal state cells. Epithelial cells are polarized cells that interact with other epithelial cells and the basal lamina which supports them. A change in the cell phenotype occurs as cells undergo alterations in their surface, cytoskeletal and extracellular matrix (ECM) markers due to changes in their cell signaling pathways. Cells proceed through transition states and acquire mesenchymal features, increased motility and invasive abilities. This process is often reversible and does not terminate in a clear universal mesenchymal state. Further, evidence of EMT in vivo is complex due to the transition processes and the intermediate states. In vitro, the process is more readily observed but progress remains to be made and studies need to be rigorous since this transition is not yet fully understood (Kalluri and Weinberg 2009; Nieto et al. 2016; Yang et al. 2020).