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Biomolecules
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EMT and Cancer II
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EMT and Cancer II

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 18806

Special Issue Editor

Prof. Dr. Alan Prem Kumar

E-Mail Website
Guest Editor
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore
Interests: breast cancer; cancer therapeutics; Wnt signaling; PI3K/Akt signaling; hippo pathway; drug development; biomarker identification; transcription factors; sumoylation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following a very successful first run, we are pleased to announce the launch of a second edition of our Special Issue on “EMT and Cancer”.

Epithelial-to-mesenchymal transition (EMT) is a crucial mechanism whose role has been explored and defined in both normal and pathological conditions. EMT is a mechanism which is tightly regulated by a variety of molecular pathways whereby epithelial cells obtain more motility by losing their apical–basal polarity and acquiring a front-near polarity that is the characteristic feature of mesenchymal cells. In spite of being vital for some of the normal processes, cancer cells use the EMT mechanism to enhance their progression and malignancy. However, more knowledge about the role of EMT in metastasis, its control, and its reversion is necessary. To address current and future perspectives in EMT in cancer, we invite authors to submit research or review articles describing recent findings in the pathology, EMT inducers and their corresponding pathways, EMT involvement in metastasis and drug resistance, Chromatin remodeling, mitochondrial remodeling, senescence, and therapeutic perspectives. Cutting-edge studies on therapeutics development and preventive strategies against EMT are highly welcome.

Potential topics in this Special Issue include but are not limited to the following:

  1. Tumor progression with metastatic expansion;
  2. Generation of tumor cells with stem cell properties;
  3. Disruption of cell–cell adhesion and cellular polarity;
  4. Remodeling of the cytoskeleton;
  5. Changes in cell–matrix adhesion;
  6. Tumor microenvironment;
  7. Non-coding RNAs;
  8. Chromatin remodeling and epigenetic modifications;
  9. Regulatory networks involving transcriptional control.

Prof. Dr. Alan Prem Kumar
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • EMT and MET
  • cancer progression
  • tumor microenvironment
  • tumor metastasis
  • cytoskeletal changes
  • transcription factors
  • mitochondrial remodeling
  • senescence

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Related Special Issue

Published Papers (6 papers)

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Research

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16 pages, 2752 KiB  
Article
2,3,5,6-Tetramethylpyrazine Targets Epithelial-Mesenchymal Transition by Abrogating Manganese Superoxide Dismutase Expression and TGFβ-Driven Signaling Cascades in Colon Cancer Cells
by Young Yun Jung, Chakrabhavi Dhananjaya Mohan, Huiyan Eng, Acharan S. Narula, Ojas A. Namjoshi, Bruce E. Blough, Kanchugarakoppal S. Rangappa, Gautam Sethi, Alan Prem Kumar and Kwang Seok Ahn
Biomolecules 2022, 12(7), 891; https://doi.org/10.3390/biom12070891 - 25 Jun 2022
Cited by 14 | Viewed by 2750
Abstract
Epithelial-mesenchymal transition (EMT) is a crucial process in which the polarized epithelial cells acquire the properties of mesenchymal cells and gain invasive properties. We have previously demonstrated that manganese superoxide dismutase (MnSOD) can regulate the EMT phenotype by modulating the intracellular reactive oxygen [...] Read more.
Epithelial-mesenchymal transition (EMT) is a crucial process in which the polarized epithelial cells acquire the properties of mesenchymal cells and gain invasive properties. We have previously demonstrated that manganese superoxide dismutase (MnSOD) can regulate the EMT phenotype by modulating the intracellular reactive oxygen species. In this report, we have demonstrated the EMT-suppressive effects of 2,3,5,6-Tetramethylpyrazine (TMP, an alkaloid isolated from Chuanxiong) in colon cancer cells. TMP suppressed the expression of MnSOD, fibronectin, vimentin, MMP-9, and N-cadherin with a parallel elevation of occludin and E-cadherin in unstimulated and TGFβ-stimulated cells. Functionally, TMP treatment reduced the proliferation, migration, and invasion of colon cancer cells. TMP treatment also modulated constitutive activated as well as TGFβ-stimulated PI3K/Akt/mTOR, Wnt/GSK3/β-catenin, and MAPK signaling pathways. TMP also inhibited the EMT program in the colon cancer cells-transfected with pcDNA3-MnSOD through modulation of MnSOD, EMT-related proteins, and oncogenic pathways. Overall, these data indicated that TMP may inhibit the EMT program through MnSOD-mediated abrogation of multiple signaling events in colon cancer cells. Full article
(This article belongs to the Special Issue EMT and Cancer II)
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9 pages, 2594 KiB  
Article
Slug Mediates MRP2 Expression in Non-Small Cell Lung Cancer Cells
by Xieyi Zhang, Wangyang Liu, Kazue Edaki, Yuta Nakazawa, Saori Takahashi, Hiroki Sunakawa, Kenta Mizoi and Takuo Ogihara
Biomolecules 2022, 12(6), 806; https://doi.org/10.3390/biom12060806 - 9 Jun 2022
Cited by 6 | Viewed by 2726
Abstract
Transcriptional factors, such as Snail, Slug, and Smuc, that cause epithelial-mesenchymal transition are thought to regulate the expression of Ezrin, Radixin, and Moesin (ERM proteins), which serve as anchors for efflux transporters on the plasma membrane surface. Our previous results using lung cancer [...] Read more.
Transcriptional factors, such as Snail, Slug, and Smuc, that cause epithelial-mesenchymal transition are thought to regulate the expression of Ezrin, Radixin, and Moesin (ERM proteins), which serve as anchors for efflux transporters on the plasma membrane surface. Our previous results using lung cancer clinical samples indicated a correlation between Slug and efflux transporter MRP2. In the current study, we aimed to evaluate the relationships between MRP2, ERM proteins, and Slug in lung cancer cells. HCC827 cells were transfected by Mock and Slug plasmid. Both mRNA expression levels and protein expression levels were measured. Then, the activity of MRP2 was evaluated using CDCF and SN-38 (MRP2 substrates). HCC827 cells transfected with the Slug plasmid showed significantly higher mRNA expression levels of MRP2 than the Mock-transfected cells. However, the mRNA expression levels of ERM proteins did not show a significant difference between Slug-transfected cells and Mock-transfected cells. Protein expression of MRP2 was increased in Slug-transfected cells. The uptake of both CDCF and SN-38 was significantly decreased after transfection with Slug. This change was abrogated by treatment with MK571, an MRP2 inhibitor. The viability of Slug-transfected cells, compared to Mock cells, significantly increased after incubation with SN-38. Thus, Slug may increase the mRNA and protein expression of MRP2 without regulation by ERM proteins in HCC827 cells, thereby enhancing MRP2 activity. Inhibition of Slug may reduce the efficacy of multidrug resistance in lung cancer. Full article
(This article belongs to the Special Issue EMT and Cancer II)
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13 pages, 2415 KiB  
Article
Relevance of A Disintegrin and Metalloproteinase Domain-Containing (ADAM)9 Protein Expression to Bladder Cancer Malignancy
by Michika Moriwaki, Trang Thi-Huynh Le, Shian-Ying Sung, Yura Jotatsu, Youngmin Yang, Yuto Hirata, Aya Ishii, Yi-Te Chiang, Kuan-Chou Chen, Katsumi Shigemura and Masato Fujisawa
Biomolecules 2022, 12(6), 791; https://doi.org/10.3390/biom12060791 - 6 Jun 2022
Cited by 3 | Viewed by 2737
Abstract
We evaluated the effect of A Disintegrin and Metalloproteinase Domain-Containing (ADAM)9 protein on exacerbation in bladder cancer KK47 and T24. First, we knocked down ADAM9 and investigated cell proliferation, migration, cell cycle, and the epithelial–mesenchymal transition (EMT)-related proteins expression in vitro. We then [...] Read more.
We evaluated the effect of A Disintegrin and Metalloproteinase Domain-Containing (ADAM)9 protein on exacerbation in bladder cancer KK47 and T24. First, we knocked down ADAM9 and investigated cell proliferation, migration, cell cycle, and the epithelial–mesenchymal transition (EMT)-related proteins expression in vitro. We then investigated the expression level of ADAM9 in clinical urine cytology samples and the Cancer Genome Atlas (TCGA) data. Cell proliferation was significantly reduced in both cell lines after ADAM9 knockdown. In the cell-cycle assay, the percentage of G0/G1 cells was significantly increased in ADAM9 knockdown T24. Migration of T24 was more strongly suppressed than KK47. The expression level of EMT-related proteins suggested that EMT was suppressed in ADAM9 knockdown T24. TCGA analysis revealed that ADAM9 mRNA expression was significantly higher in stage IV and high-grade cancer than in other stages and low-grade cancer. Moreover, in the gene expression omnibus (GEO) study, bladder cancer with surrounding carcinoma and invasive carcinoma showed significantly high ADAM9 mRNA expression. We found that ADAM9 knockdown suppressed cell proliferation and migration in bladder cancer and that high-grade bladder cancer is correlated with higher expression of ADAM9. Full article
(This article belongs to the Special Issue EMT and Cancer II)
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Review

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15 pages, 1202 KiB  
Review
Stromal-Modulated Epithelial-to-Mesenchymal Transition in Cancer Cells
by Huda I. Atiya, Grace Gorecki, Geyon L. Garcia, Leonard G. Frisbie, Roja Baruwal and Lan Coffman
Biomolecules 2023, 13(11), 1604; https://doi.org/10.3390/biom13111604 - 1 Nov 2023
Cited by 11 | Viewed by 2733
Abstract
The ability of cancer cells to detach from the primary site and metastasize is the main cause of cancer- related death among all cancer types. Epithelial-to-mesenchymal transition (EMT) is the first event of the metastatic cascade, resulting in the loss of cell–cell adhesion [...] Read more.
The ability of cancer cells to detach from the primary site and metastasize is the main cause of cancer- related death among all cancer types. Epithelial-to-mesenchymal transition (EMT) is the first event of the metastatic cascade, resulting in the loss of cell–cell adhesion and the acquisition of motile and stem-like phenotypes. A critical modulator of EMT in cancer cells is the stromal tumor microenvironment (TME), which can promote the acquisition of a mesenchymal phenotype through direct interaction with cancer cells or changes to the broader microenvironment. In this review, we will explore the role of stromal cells in modulating cancer cell EMT, with particular emphasis on the function of mesenchymal stromal/stem cells (MSCs) through the activation of EMT-inducing pathways, extra cellular matrix (ECM) remodeling, immune cell alteration, and metabolic rewiring. Full article
(This article belongs to the Special Issue EMT and Cancer II)
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22 pages, 2712 KiB  
Review
Regulation of the Epithelial to Mesenchymal Transition in Osteosarcoma
by Kristin Hinton, Andrew Kirk, Paulose Paul and Sujata Persad
Biomolecules 2023, 13(2), 398; https://doi.org/10.3390/biom13020398 - 20 Feb 2023
Cited by 9 | Viewed by 3897
Abstract
The epithelial to mesenchymal transition (EMT) is a cellular process that has been linked to the promotion of aggressive cellular features in many cancer types. It is characterized by the loss of the epithelial cell phenotype and a shift to a more mesenchymal [...] Read more.
The epithelial to mesenchymal transition (EMT) is a cellular process that has been linked to the promotion of aggressive cellular features in many cancer types. It is characterized by the loss of the epithelial cell phenotype and a shift to a more mesenchymal phenotype and is accompanied by an associated change in cell markers. EMT is highly complex and regulated via multiple signaling pathways. While the importance of EMT is classically described for carcinomas—cancers of epithelial origin—it has also been clearly demonstrated in non-epithelial cancers, including osteosarcoma (OS), a primary bone cancer predominantly affecting children and young adults. Recent studies examining EMT in OS have highlighted regulatory roles for multiple proteins, non-coding nucleic acids, and components of the tumor micro-environment. This review serves to summarize these experimental findings, identify key families of regulatory molecules, and identify potential therapeutic targets specific to the EMT process in OS. Full article
(This article belongs to the Special Issue EMT and Cancer II)
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15 pages, 1330 KiB  
Review
Current Progress of EMT: A New Direction of Targeted Therapy for Colorectal Cancer with Invasion and Metastasis
by Zhuomin Tan, Wenyan Sun, Ya Li, Xingmeng Jiao, Mingliang Zhu, Junfei Zhang, Chen Qing and Yinnong Jia
Biomolecules 2022, 12(12), 1723; https://doi.org/10.3390/biom12121723 - 22 Nov 2022
Cited by 24 | Viewed by 3062
Abstract
Colorectal cancer (CRC) is a common malignant tumor with a high frequency of recurrence and metastasis, which are the major causes of death in patients. The prerequisite for the invasion and metastasis is the strong mobility of CRC cells to transport far away [...] Read more.
Colorectal cancer (CRC) is a common malignant tumor with a high frequency of recurrence and metastasis, which are the major causes of death in patients. The prerequisite for the invasion and metastasis is the strong mobility of CRC cells to transport far away from the original site to the distant organs and tissues, where they settle down and proliferate. It was reported that the epithelial-mesenchymal transition (EMT) is involved in the occurrence and development of various tumors in the entire process of tumor invasion and metastasis. Therefore, as a vital factor for the biological characteristics of tumor cells, EMT markers may serve as prognostic predictors and potential therapeutic targets in CRC. This article mainly reviews the current status of CRC with metastasis, the studies of EMT, the possible relationship of EMT with CRC, as well as the potential targeted therapy. Full article
(This article belongs to the Special Issue EMT and Cancer II)
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