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Molecular Regulation of Cancer Cell Migration, Invasion, and Metastasis 2.0
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Molecular Regulation of Cancer Cell Migration, Invasion, and Metastasis 2.0

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: closed (30 November 2023) | Viewed by 6920

Special Issue Editor

Dr. Andrea Disanza

E-Mail Website
Guest Editor
IFOM, FIRC Institute of Molecular Oncology, Via Adamello 16, 20139 Milan, Italy
Interests: actin and membrane dynamics; tumor cell migration and invasion
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer metastasis represents an advanced stage of malignancy and is the leading cause of cancer- therapeutic failure and related deaths. Metastasis is a multistep process that includes loss of cell polarity, tissue disorganization, and cancer cell migration and invasion, which are all hallmarks of cancer. To spread through the tissues and disseminate faraway, tumor cells use mechanisms involving several molecular actors: adhesion receptors, receptor tyrosine kinases, cytoskeleton proteins, and adapter and signaling proteins. An overarching feature of malignant progression, particularly in the case of carcinoma (i.e., epithelia-derived solid cancer), is the acquisition of cell migration. Carcinoma can take a variety of different, frequently interchangeable modes of migration that drive the dissemination of individual or collective entities. The concept of migratory plasticity has emerged as dominant in oncology. The intent of this Special Issue on “Molecular Regulation of Cancer Cell Migration, Invasion, and Metastasis” is to dissect the molecular mechanisms at the base of cancer cell migration and invasion strategies. Therefore, we warmly welcome submissions, including original papers and reviews, on this widely discussed topic.

Dr. Andrea Disanza
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • signaling
  • cell polarity
  • migration
  • invasion
  • adhesions
  • cell protrusions
  • membrane and actin dynamics

Published Papers (4 papers)

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Research

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16 pages, 4973 KiB  
Article
An Increase in Mucin2 Expression Is Required for Colon Cancer Progression Mediated by L1
by Arka Saha, Nancy Gavert, Thomas Brabletz and Avri Ben-Ze’ev
Int. J. Mol. Sci. 2023, 24(17), 13418; https://doi.org/10.3390/ijms241713418 - 30 Aug 2023
Viewed by 1053
Abstract
An induction in the expression of the cell adhesion receptor L1, a Wnt target gene, is a characteristic feature of Wnt/β-catenin activation in colon cancer cells at later stages of the disease. We investigated the proteins secreted following L1 expression in colon cancer [...] Read more.
An induction in the expression of the cell adhesion receptor L1, a Wnt target gene, is a characteristic feature of Wnt/β-catenin activation in colon cancer cells at later stages of the disease. We investigated the proteins secreted following L1 expression in colon cancer cells and identified Mucin2 among the most abundant secreted proteins. We found that suppressing Mucin2 expression in L1-expressing colon cancer cells inhibits cell proliferation, motility, tumorigenesis, and liver metastasis. We detected several signaling pathways involved in Mucin2 induction in L1-expressing cells. In human colon cancer tissue, Mucin2 expression was significantly reduced or lost in the adenocarcinoma tissue, while in the mucinous subtype of colon cancer tissue, Mucin2 expression was increased. An increased signature of L1/Mucin2 expression reduced the survival rate of human colon cancer patients. Thus, induction of Mucin2 expression by L1 is required during mucinous colon cancer progression and can serve as a marker for diagnosis and a target for therapy. Full article
(This article belongs to the Special Issue Molecular Regulation of Cancer Cell Migration, Invasion, and Metastasis 2.0)
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Review

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24 pages, 4124 KiB  
Review
Can CD133 Be Regarded as a Prognostic Biomarker in Oncology: Pros and Cons
by Alisa Gisina, Yan Kim, Konstantin Yarygin and Alexey Lupatov
Int. J. Mol. Sci. 2023, 24(24), 17398; https://doi.org/10.3390/ijms242417398 - 12 Dec 2023
Cited by 1 | Viewed by 1197
Abstract
The CD133 cell membrane glycoprotein, also termed prominin-1, is expressed on some of the tumor cells of both solid and blood malignancies. The CD133-positive tumor cells were shown to exhibit higher proliferative activity, greater chemo- and radioresistance, and enhanced tumorigenicity compared to their [...] Read more.
The CD133 cell membrane glycoprotein, also termed prominin-1, is expressed on some of the tumor cells of both solid and blood malignancies. The CD133-positive tumor cells were shown to exhibit higher proliferative activity, greater chemo- and radioresistance, and enhanced tumorigenicity compared to their CD133-negative counterparts. For this reason, CD133 is regarded as a potential prognostic biomarker in oncology. The CD133-positive cells are related to the cancer stem cell subpopulation in many types of cancer. Recent studies demonstrated the involvement of CD133 in the regulation of proliferation, autophagy, and apoptosis in cancer cells. There is also evidence of its participation in the epithelial–mesenchymal transition associated with tumor progression. For a number of malignant tumor types, high CD133 expression is associated with poor prognosis, and the prognostic significance of CD133 has been confirmed in a number of meta-analyses. However, some published papers suggest that CD133 has no prognostic significance or even demonstrate a certain correlation between high CD133 levels and a positive prognosis. This review summarizes and discusses the existing evidence for and against the prognostic significance of CD133 in cancer. We also consider possible reasons for conflicting findings from the studies of the clinical significance of CD133. Full article
(This article belongs to the Special Issue Molecular Regulation of Cancer Cell Migration, Invasion, and Metastasis 2.0)
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17 pages, 2926 KiB  
Review
Intratumor Heterogeneity and Treatment Resistance of Solid Tumors with a Focus on Polyploid/Senescent Giant Cancer Cells (PGCCs)
by Razmik Mirzayans and David Murray
Int. J. Mol. Sci. 2023, 24(14), 11534; https://doi.org/10.3390/ijms241411534 - 16 Jul 2023
Cited by 5 | Viewed by 2131
Abstract
Single cell biology has revealed that solid tumors and tumor-derived cell lines typically contain subpopulations of cancer cells that are readily distinguishable from the bulk of cancer cells by virtue of their enormous size. Such cells with a highly enlarged nucleus, multiple nuclei, [...] Read more.
Single cell biology has revealed that solid tumors and tumor-derived cell lines typically contain subpopulations of cancer cells that are readily distinguishable from the bulk of cancer cells by virtue of their enormous size. Such cells with a highly enlarged nucleus, multiple nuclei, and/or multiple micronuclei are often referred to as polyploid giant cancer cells (PGCCs), and may exhibit features of senescence. PGCCs may enter a dormant phase (active sleep) after they are formed, but a subset remain viable, secrete growth promoting factors, and can give rise to therapy resistant and tumor repopulating progeny. Here we will briefly discuss the prevalence and prognostic value of PGCCs across different cancer types, the current understanding of the mechanisms of their formation and fate, and possible reasons why these tumor repopulating “monsters” continue to be ignored in most cancer therapy-related preclinical studies. In addition to PGCCs, other subpopulations of cancer cells within a solid tumor (such as oncogenic caspase 3-activated cancer cells and drug-tolerant persister cancer cells) can also contribute to therapy resistance and pose major challenges to the delivery of cancer therapy. Full article
(This article belongs to the Special Issue Molecular Regulation of Cancer Cell Migration, Invasion, and Metastasis 2.0)
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44 pages, 3109 KiB  
Review
Regulative Roles of Metabolic Plasticity Caused by Mitochondrial Oxidative Phosphorylation and Glycolysis on the Initiation and Progression of Tumorigenesis
by Nan Niu, Jinfeng Ye, Zhangli Hu, Junbin Zhang and Yun Wang
Int. J. Mol. Sci. 2023, 24(8), 7076; https://doi.org/10.3390/ijms24087076 - 11 Apr 2023
Cited by 4 | Viewed by 1992
Abstract
One important feature of tumour development is the regulatory role of metabolic plasticity in maintaining the balance of mitochondrial oxidative phosphorylation and glycolysis in cancer cells. In recent years, the transition and/or function of metabolic phenotypes between mitochondrial oxidative phosphorylation and glycolysis in [...] Read more.
One important feature of tumour development is the regulatory role of metabolic plasticity in maintaining the balance of mitochondrial oxidative phosphorylation and glycolysis in cancer cells. In recent years, the transition and/or function of metabolic phenotypes between mitochondrial oxidative phosphorylation and glycolysis in tumour cells have been extensively studied. In this review, we aimed to elucidate the characteristics of metabolic plasticity (emphasizing their effects, such as immune escape, angiogenesis migration, invasiveness, heterogeneity, adhesion, and phenotypic properties of cancers, among others) on tumour progression, including the initiation and progression phases. Thus, this article provides an overall understanding of the influence of abnormal metabolic remodeling on malignant proliferation and pathophysiological changes in carcinoma. Full article
(This article belongs to the Special Issue Molecular Regulation of Cancer Cell Migration, Invasion, and Metastasis 2.0)
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