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Cancers
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Mucins and Cancers
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Mucins and Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (25 November 2023) | Viewed by 16224

Special Issue Editor

Prof. Dr. Vasso Apostolopoulos

E-Mail Website
Guest Editor
Institute for Health and Sport, Victoria University, Melbourne, VIC 3011, Australia
Interests: immunology; protein crystallography; medicinal chemistry; cellular and molecular biology; extensive translational research; clinical trials; vaccines; drugs; healthy ageing; chronic diseases; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

From the late 1980s to the early 1990s, mucins were identified to play a key role on cancer cells. The first mucin to be identified was human MUC1 expressed on epithelial cells and overexpressed on adenocarcinomas. By the mid-1990s, human clinical trials were conducted in cancer patients with the aim of targeting immune responses to MUC1. Soon after, other mucins were identified, such as MUC2, MUC3, MUC4, MUC5, MUC6, and MUC21. The aberrant expression of some of these mucins—including MUC1, MUC4, MUC13, and MUC16—are also associated with diverse human malignancies. Mucins are also associated with the diagnosis, metastatic progression, prognosis outcomes, inflammation, function, therapy, and development of drugs and vaccines. In this Special Issue, we celebrate over 30 years of mucins in research, especially studies that have shown links between mucins and cancer. I invite you to submit an article to this Special Issue. We look forward to receiving your contributions.

Prof. Dr. Vasso Apostolopoulos
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 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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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

  • mucin
  • cancer
  • vaccine
  • disease
  • immunotherapy
  • drug development
  • inflammation
  • cancer therapy
  • cancer prognosis
  • immunomodulation
  • diagnosis
  • biomarker

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Published Papers (5 papers)

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Research

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21 pages, 5447 KiB  
Article
Differential Gene Expression of Checkpoint Markers and Cancer Markers in Mouse Models of Spontaneous Chronic Colitis
by Ramya Ephraim, Sarah Fraser, Jeannie Devereaux, Rhian Stavely, Jack Feehan, Rajaraman Eri, Kulmira Nurgali and Vasso Apostolopoulos
Cancers 2023, 15(19), 4793; https://doi.org/10.3390/cancers15194793 - 29 Sep 2023
Cited by 2 | Viewed by 2268
Abstract
The presence of checkpoint markers in cancer cells aids in immune escape. The identification of checkpoint markers and early cancer markers is of utmost importance to gain clarity regarding the relationship between colitis and progressive inflammation leading to cancer. Herein, the gene expression [...] Read more.
The presence of checkpoint markers in cancer cells aids in immune escape. The identification of checkpoint markers and early cancer markers is of utmost importance to gain clarity regarding the relationship between colitis and progressive inflammation leading to cancer. Herein, the gene expression levels of checkpoint makers, cancer-related pathways, and cancer genes in colon tissues of mouse models of chronic colitis (Winnie and Winnie-Prolapse mice) using next-generation sequencing are determined. Winnie mice are a result of a Muc2 missense mutation. The identification of such genes and their subsequent expression and role at the protein level would enable novel markers for the early diagnosis of cancer in IBD patients. The differentially expressed genes in the colonic transcriptome were analysed based on the Kyoto Encyclopedia of Genes and Genomes pathway. The expression of several oncogenes is associated with the severity of IBD, with Winnie-Prolapse mice expressing a large number of key genes associated with development of cancer. This research presents a number of new targets to evaluate for the development of biomarkers and therapeutics. Full article
(This article belongs to the Special Issue Mucins and Cancers)
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14 pages, 2434 KiB  
Article
Prevention of Inflammation-Driven Colon Carcinogenesis in Human MUC1 Transgenic Mice by Vaccination with MUC1 DNA and Dendritic Cells
by Retno Murwanti, Kaori Denda-Nagai, Daisuke Sugiura, Kaoru Mogushi, Sandra J. Gendler and Tatsuro Irimura
Cancers 2023, 15(6), 1920; https://doi.org/10.3390/cancers15061920 - 22 Mar 2023
Cited by 2 | Viewed by 2534
Abstract
The preventive efficacy of MUC1-specific DNA immunization on inflammation-driven colon carcinogenesis in human MUC1 transgenic (MUC1.Tg) mice was investigated. Mice were vaccinated with MUC1 DNA mixed with autologous bone-marrow-derived dendritic cells (BMDCs), and then colonic tumors were induced by azoxymethane (AOM) injection [...] Read more.
The preventive efficacy of MUC1-specific DNA immunization on inflammation-driven colon carcinogenesis in human MUC1 transgenic (MUC1.Tg) mice was investigated. Mice were vaccinated with MUC1 DNA mixed with autologous bone-marrow-derived dendritic cells (BMDCs), and then colonic tumors were induced by azoxymethane (AOM) injection and oral administration of dextran sulfate sodium (DSS). Two types of tumors, squamous metaplasia and tubular adenoma, were observed. Both expressed high levels of MUC1 as indicated by the binding of anti-MUC1 antibodies with different specificities, whereas MUC1 expression was not detected in normal colonic mucosa. When mice were immunized with MUC1 DNA + BMDCs, tumor incidence, tumor number, and tumor size were significantly reduced. In contrast, vaccination with MUC1 DNA alone or BMDCs alone was ineffective in reducing tumor burden. Inflammation caused by DSS was not suppressed by the MUC1 DNA + BMDCs vaccination. Furthermore, MUC1 protein expression levels, as judged by anti-MUC1 antibody binding in tumors grown after vaccination, did not significantly differ from the control. In conclusion, an inflammation-driven carcinogenesis model was established in MUC1.Tg mice, closely resembling human colon carcinogenesis. In this model, vaccination with MUC1 DNA + BMDCs was effective in overriding MUC1 tolerance and reducing the tumor burden by a mechanism not affecting the level of colonic inflammation. Full article
(This article belongs to the Special Issue Mucins and Cancers)
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Review

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15 pages, 1736 KiB  
Review
Galectin-3 and Epithelial MUC1 Mucin—Interactions Supporting Cancer Development
by Iwona Radziejewska
Cancers 2023, 15(10), 2680; https://doi.org/10.3390/cancers15102680 - 9 May 2023
Cited by 5 | Viewed by 2617
Abstract
Aberrant glycosylation of cell surface proteins is a very common feature of many cancers. One of the glycoproteins, which undergoes specific alterations in the glycosylation of tumor cells is epithelial MUC1 mucin, which is highly overexpressed in the malignant state. Such changes lead [...] Read more.
Aberrant glycosylation of cell surface proteins is a very common feature of many cancers. One of the glycoproteins, which undergoes specific alterations in the glycosylation of tumor cells is epithelial MUC1 mucin, which is highly overexpressed in the malignant state. Such changes lead to the appearance of tumor associated carbohydrate antigens (TACAs) on MUC1, which are rarely seen in healthy cells. One of these structures is the Thomsen-Friedenreich disaccharide Galβ1-3GalNAc (T or TF antigen), which is typical for about 90% of cancers. It was revealed that increased expression of the T antigen has a big impact on promoting cancer progression and metastasis, among others, due to the interaction of this antigen with the β-galactose binding protein galectin-3 (Gal-3). In this review, we summarize current information about the interactions between the T antigen on MUC1 mucin and Gal-3, and their impact on cancer progression and metastasis. Full article
(This article belongs to the Special Issue Mucins and Cancers)
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22 pages, 7487 KiB  
Review
The Mucin Family of Proteins: Candidates as Potential Biomarkers for Colon Cancer
by Kristin E. Cox, Shanglei Liu, Thinzar M. Lwin, Robert M. Hoffman, Surinder K. Batra and Michael Bouvet
Cancers 2023, 15(5), 1491; https://doi.org/10.3390/cancers15051491 - 27 Feb 2023
Cited by 27 | Viewed by 5003
Abstract
Mucins (MUC1–MUC24) are a family of glycoproteins involved in cell signaling and barrier protection. They have been implicated in the progression of numerous malignancies including gastric, pancreatic, ovarian, breast, and lung cancer. Mucins have also been extensively studied with respect to colorectal cancer. [...] Read more.
Mucins (MUC1–MUC24) are a family of glycoproteins involved in cell signaling and barrier protection. They have been implicated in the progression of numerous malignancies including gastric, pancreatic, ovarian, breast, and lung cancer. Mucins have also been extensively studied with respect to colorectal cancer. They have been found to have diverse expression profiles amongst the normal colon, benign hyperplastic polyps, pre-malignant polyps, and colon cancers. Those expressed in the normal colon include MUC2, MUC3, MUC4, MUC11, MUC12, MUC13, MUC15 (at low levels), and MUC21. Whereas MUC5, MUC6, MUC16, and MUC20 are absent from the normal colon and are expressed in colorectal cancers. MUC1, MUC2, MUC4, MUC5AC, and MUC6 are currently the most widely covered in the literature regarding their role in the progression from normal colonic tissue to cancer. Full article
(This article belongs to the Special Issue Mucins and Cancers)
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15 pages, 2708 KiB  
Review
Emergence of MUC1 in Mammals for Adaptation of Barrier Epithelia
by Donald W. Kufe
Cancers 2022, 14(19), 4805; https://doi.org/10.3390/cancers14194805 - 30 Sep 2022
Cited by 16 | Viewed by 2758
Abstract
The mucin 1 (MUC1) gene was discovered based on its overexpression in human breast cancers. Subsequent work demonstrated that MUC1 is aberrantly expressed in cancers originating from other diverse organs, including skin and immune cells. These findings supported a role for [...] Read more.
The mucin 1 (MUC1) gene was discovered based on its overexpression in human breast cancers. Subsequent work demonstrated that MUC1 is aberrantly expressed in cancers originating from other diverse organs, including skin and immune cells. These findings supported a role for MUC1 in the adaptation of barrier tissues to infection and environmental stress. Of fundamental importance for this evolutionary adaptation was inclusion of a SEA domain, which catalyzes autoproteolysis of the MUC1 protein and formation of a non-covalent heterodimeric complex. The resulting MUC1 heterodimer is poised at the apical cell membrane to respond to loss of homeostasis. Disruption of the complex releases the MUC1 N-terminal (MUC1-N) subunit into a protective mucous gel. Conversely, the transmembrane C-terminal (MUC1-C) subunit activates a program of lineage plasticity, epigenetic reprogramming and repair. This MUC1-C-activated program apparently evolved for barrier tissues to mount self-regulating proliferative, inflammatory and remodeling responses associated with wound healing. Emerging evidence indicates that MUC1-C underpins inflammatory adaptation of tissue stem cells and immune cells in the barrier niche. This review focuses on how prolonged activation of MUC1-C by chronic inflammation in these niches promotes the cancer stem cell (CSC) state by establishing auto-inductive nodes that drive self-renewal and tumorigenicity. Full article
(This article belongs to the Special Issue Mucins and Cancers)
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