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Cellular Plasticity, Epithelial-Mesenchymal Transition and Metastasis
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Cellular Plasticity, Epithelial-Mesenchymal Transition and Metastasis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 February 2025 | Viewed by 9229

Special Issue Editor

Prof. Dr. Martin Schreiber

E-Mail Website
Guest Editor
Department of Obstetrics & Gynecology, Medical University of Vienna, 1090 Vienna, Austria
Interests: breast cancer; diagnostic and prognostic markers; gene expression; transcriptional regulation; genomics and transcriptomics; p53 pathway; hormone receptor pathways; epithelial-mesenchymal transition
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epithelial to mesenchymal transition (EMT) is a physiological transdifferentiation program by which epithelial cells undergo profound phenotypic and molecular changes to gradually lose their polarized epithelial morphology and expression of epithelial genes, specifically cell adhesion and epithelial polarity molecules. Instead, they acquire the fibroblastoid morphology, gene expression programs, and higher motility of mesenchymal cells. EMT plays crucial roles in embryogenesis and in the formation of the body plan. In addition, EMT can also be activated transiently or stably, and to different degrees, by epithelial cancer cells, which endows them with migratory, inva­sive, and cancer stem cell properties, increasing their resistance to apoptosis and chemotherapy in addition to enabling them to metastasize; however, aspects of EMT are also activated in non-epithelial cancer cells, as well as in fibrosis. EMT in development and cancer is typically regulated by several core transcription factors (SNAI1/2, ZEB1/2, and TWIST1), which are frequently upregulated in various combinations during EMT. Cancer cells often undergo partial rather than complete EMT, thus attaining a cellular phenotype along the epithelial–mesenchymal continuum and exhibiting both epithelial and mesenchymal properties. Partial EMT is thought to increase cellular plasticity and adaptability as well as invasive and metastatic capacity, whereas more complete EMT is thought to be associated with resistance to chemotherapy.

This Special Issue intends to bridge the gap between functional studies in in vitro and in vivo models of EMT and demonstrations of EMT in clinical (tumor) samples and their association with motility, invasiveness, metastasis, chemoresistance, and cancer cell stemness. Submissions of research articles and reviews covering all aspects of EMT, cellular plasticity, and/or metastasis are welcome.

Prof. Dr. Martin Schreiber
Guest Editor

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Keywords

  • epithelial–mesenchymal transition (EMT)
  • partial vs. full EMT
  • cellular plasticity
  • EMT in physiology and development
  • cancer
  • fibrosis
  • invasion and metastasis

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Published Papers (5 papers)

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Research

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19 pages, 2906 KiB  
Article
TGF-β-Induced PAUF Plays a Pivotal Role in the Migration and Invasion of Human Pancreatic Ductal Adenocarcinoma Cell Line Panc-1
by Miso Lee, Hyejun Ham, Jiyeong Lee, Eun Soo Lee, Choon Hee Chung, Deok-Hoon Kong, Jeong-Ran Park and Dong-Keon Lee
Int. J. Mol. Sci. 2024, 25(21), 11420; https://doi.org/10.3390/ijms252111420 - 24 Oct 2024
Viewed by 810
Abstract
Pancreatic adenocarcinoma upregulated factor (PAUF) was initially identified as a secreted protein that is substantially expressed in pancreatic ductal adenocarcinoma (PDAC). PAUF also affects invasiveness, motility, and the proliferation of cells in several types of cancer. Recently, PAUF was reported to play a [...] Read more.
Pancreatic adenocarcinoma upregulated factor (PAUF) was initially identified as a secreted protein that is substantially expressed in pancreatic ductal adenocarcinoma (PDAC). PAUF also affects invasiveness, motility, and the proliferation of cells in several types of cancer. Recently, PAUF was reported to play a pivotal role in the TLR4-mediated migration and invasion of PDAC cells. However, the mechanism inducing PAUF expression and its functional role in TGF-β-stimulated PDAC cells have not yet been studied. Thus, we first assessed whether TGF-β regulates PAUF expression in several PDAC cell lines and found a significant increase in PAUF expression in Smad signaling-positive Panc-1 cells treated with TGF-β. We also found that the PAUF promoter region contains a Smad-binding element. TGF-β-treated Panc-1 cells showed an increase in PAUF promoter activity, but this effect was not observed in TGF-β-stimulated Smad4-null BxPC-3 cells. Restoring Smad4 expression increased the PAUF promoter activity and expression in Smad4-overexpressing BxPC-3 cells treated with TGF-β. We further found that PAUF aggravated the TGF-β-induced epithelial–mesenchymal transition (EMT) in Panc-1 and BxPC-3 cells via the activation of MEK-ERK signaling. These results indicate that TGF-β/Smad signaling-mediated upregulation of PAUF plays a crucial role in EMT progression by activating the TGF-β-mediated MEK-ERK signaling pathway. Full article
(This article belongs to the Special Issue Cellular Plasticity, Epithelial-Mesenchymal Transition and Metastasis)
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23 pages, 5052 KiB  
Article
Co-Expression Network Analysis Unveiled lncRNA-mRNA Links Correlated to Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor Resistance and/or Intermediate Epithelial-to-Mesenchymal Transition Phenotypes in a Human Non-Small Cell Lung Cancer Cellular Model System
by Valentina Fustaino, Giuliana Papoff, Francesca Ruberti and Giovina Ruberti
Int. J. Mol. Sci. 2024, 25(7), 3863; https://doi.org/10.3390/ijms25073863 - 29 Mar 2024
Cited by 1 | Viewed by 1812
Abstract
We investigated mRNA-lncRNA co-expression patterns in a cellular model system of non-small cell lung cancer (NSCLC) sensitive and resistant to the epithelial growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) erlotinib/gefitinib. The aim of this study was to unveil insights into the complex [...] Read more.
We investigated mRNA-lncRNA co-expression patterns in a cellular model system of non-small cell lung cancer (NSCLC) sensitive and resistant to the epithelial growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) erlotinib/gefitinib. The aim of this study was to unveil insights into the complex mechanisms of NSCLC targeted therapy resistance and epithelial-to-mesenchymal transition (EMT). Genome-wide RNA expression was quantified for weighted gene co-expression network analysis (WGCNA) to correlate the expression levels of mRNAs and lncRNAs. Functional enrichment analysis and identification of lncRNAs were conducted on modules associated with the EGFR-TKI response and/or intermediate EMT phenotypes. We constructed lncRNA-mRNA co-expression networks and identified key modules and their enriched biological functions. Processes enriched in the selected modules included RHO (A, B, C) GTPase and regulatory signaling pathways, apoptosis, inflammatory and interleukin signaling pathways, cell adhesion, cell migration, cell and extracellular matrix organization, metabolism, and lipid metabolism. Interestingly, several lncRNAs, already shown to be dysregulated in cancer, are connected to a small number of mRNAs, and several lncRNAs are interlinked with each other in the co-expression network. Full article
(This article belongs to the Special Issue Cellular Plasticity, Epithelial-Mesenchymal Transition and Metastasis)
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14 pages, 9656 KiB  
Article
Therapeutic Potential of Regorafenib in Cisplatin-Resistant Bladder Cancer with High Epithelial–Mesenchymal Transition and Stemness Properties
by Feng-Che Kuan, Jhy-Ming Li, Yun-Ching Huang, Shun-Fu Chang and Chung-Sheng Shi
Int. J. Mol. Sci. 2023, 24(24), 17610; https://doi.org/10.3390/ijms242417610 - 18 Dec 2023
Cited by 1 | Viewed by 1714
Abstract
Bladder cancer is becoming one of the most common malignancies across the world. Although treatment strategy has been continuously improved, which has led to cisplatin-based chemotherapy becoming the standard medication, cancer recurrence and metastasis still occur in a high proportion of patients because [...] Read more.
Bladder cancer is becoming one of the most common malignancies across the world. Although treatment strategy has been continuously improved, which has led to cisplatin-based chemotherapy becoming the standard medication, cancer recurrence and metastasis still occur in a high proportion of patients because of drug resistance. The high efficacy of regorafenib, a broad-spectrum kinase inhibitor, has been evidenced in treating a variety of advanced cancers. Hence, this study investigated whether regorafenib could also effectively antagonize the survival of cisplatin-resistant bladder cancer and elucidate the underlying mechanism. Two types of cisplatin-resistant bladder cancer cells, T24R1 and T24R2, were isolated from T24 cisplatin-sensitive bladder cancer cells. These cells were characterized, and T24R1- and T24R2-xenografted tumor mice were created to examine the therapeutic efficacy of regorafenib. T24R1 and T24R2 cells exhibited higher expression levels of epithelial–mesenchymal transition (EMT) and stemness markers compared to the T24 cells, and regorafenib could simultaneously inhibit the viability and the expression of EMT/stemness markers of both T24R1 and T24R2 cells. Moreover, regorafenib could efficiently arrest the cell cycle, promote apoptosis, and block the transmigration/migration capabilities of both types of cells. Finally, regorafenib could significantly antagonize the growth of T24R1- and T24R2-xenografted tumors in mice. These results demonstrated the therapeutic efficacy of regorafenib in cisplatin-resistant bladder cancers. This study, thus, provides more insights into the mechanism of action of regorafenib and demonstrates its great potential in the future treatment of cisplatin-resistant advanced bladder cancer patients. Full article
(This article belongs to the Special Issue Cellular Plasticity, Epithelial-Mesenchymal Transition and Metastasis)
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Review

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47 pages, 2332 KiB  
Review
Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression
by Paulina Tomecka, Dominika Kunachowicz, Julia Górczyńska, Michał Gebuza, Jacek Kuźnicki, Katarzyna Skinderowicz and Anna Choromańska
Int. J. Mol. Sci. 2024, 25(16), 8972; https://doi.org/10.3390/ijms25168972 - 17 Aug 2024
Cited by 1 | Viewed by 2120
Abstract
Epithelial-mesenchymal transition (EMT) is a process in which an epithelial cell undergoes multiple modifications, acquiring both morphological and functional characteristics of a mesenchymal cell. This dynamic process is initiated by various inducing signals that activate numerous signaling pathways, leading to the stimulation of [...] Read more.
Epithelial-mesenchymal transition (EMT) is a process in which an epithelial cell undergoes multiple modifications, acquiring both morphological and functional characteristics of a mesenchymal cell. This dynamic process is initiated by various inducing signals that activate numerous signaling pathways, leading to the stimulation of transcription factors. EMT plays a significant role in cancer progression, such as metastasis and tumor heterogeneity, as well as in drug resistance. In this article, we studied molecular mechanisms, epigenetic regulation, and cellular plasticity of EMT, as well as microenvironmental factors influencing this process. We included both in vivo and in vitro models in EMT investigation and clinical implications of EMT, such as the use of EMT in curing oncological patients and targeting its use in therapies. Additionally, this review concludes with future directions and challenges in the wide field of EMT. Full article
(This article belongs to the Special Issue Cellular Plasticity, Epithelial-Mesenchymal Transition and Metastasis)
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22 pages, 1308 KiB  
Review
Shake It Up Baby Now: The Changing Focus on TWIST1 and Epithelial to Mesenchymal Transition in Cancer and Other Diseases
by Dureali Mirjat, Muhammad Kashif and Cai M. Roberts
Int. J. Mol. Sci. 2023, 24(24), 17539; https://doi.org/10.3390/ijms242417539 - 16 Dec 2023
Cited by 2 | Viewed by 2079
Abstract
TWIST1 is a transcription factor that is necessary for healthy neural crest migration, mesoderm development, and gastrulation. It functions as a key regulator of epithelial-to-mesenchymal transition (EMT), a process by which cells lose their polarity and gain the ability to migrate. EMT is [...] Read more.
TWIST1 is a transcription factor that is necessary for healthy neural crest migration, mesoderm development, and gastrulation. It functions as a key regulator of epithelial-to-mesenchymal transition (EMT), a process by which cells lose their polarity and gain the ability to migrate. EMT is often reactivated in cancers, where it is strongly associated with tumor cell invasion and metastasis. Early work on TWIST1 in adult tissues focused on its transcriptional targets and how EMT gave rise to metastatic cells. In recent years, the roles of TWIST1 and other EMT factors in cancer have expanded greatly as our understanding of tumor progression has advanced. TWIST1 and related factors are frequently tied to cancer cell stemness and changes in therapeutic responses and thus are now being viewed as attractive therapeutic targets. In this review, we highlight non-metastatic roles for TWIST1 and related EMT factors in cancer and other disorders, discuss recent findings in the areas of therapeutic resistance and stemness in cancer, and comment on the potential to target EMT for therapy. Further research into EMT will inform novel treatment combinations and strategies for advanced cancers and other diseases. Full article
(This article belongs to the Special Issue Cellular Plasticity, Epithelial-Mesenchymal Transition and Metastasis)
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