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Cancers
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Cell Adhesion Molecules in Metastasis
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Cell Adhesion Molecules in Metastasis

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

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 29483

Special Issue Editors

Dr. Tracey Martin

E-Mail Website
Guest Editor
Cardiff China Medical Research Collaborative, Division of Cancer & Genetics, Cardiff University, Henry Wellcome Building, Heath Park, Cardiff, CF14 4XN, UK
Interests: cancer metastasis; cell adhesion; tight junctions; blood brain barrier
Special Issues, Collections and Topics in MDPI journals
Dr. Andrew Sanders

E-Mail Website
Co-Guest Editor
Cardiff China Medical Research Collaborative, Division of Cancer & Genetics, Cardiff University, Henry Wellcome Building, Heath Park, Cardiff, CF14 4XN, UK
Interests: cancer metastasis; cell adhesion; eplin; ALCAM

Special Issue Information

Metastatic disease accounts for the majority of cancer-related deaths and remains a significant problem in the management and treatment of patients. The process of metastasis is complex, with a vast array of related components and complex interactions involved in progression through the metastatic cascade. It has long been established that cell adhesion molecules play significant roles in this process and are often dysregulated or disrupted during cancer progression. This has resulted in a great deal of scientific attention focusing on the potential of various cell adhesion molecules as cancer biomarkers or prognostic factors and in understanding their role and associated regulatory mechanisms in cancer progression.

The current Special Issue will focus on furthering our understanding of cell adhesion molecules and their importance in cancer metastasis.

Dr. Tracey Martin
Guest Editor
Dr. Andrew Sanders
Co-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. 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

  • cell adhesion
  • cell junctions
  • metastasis
  • cancer
  • targets
  • mechanism

Published Papers (7 papers)

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Research

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21 pages, 11262 KiB  
Article
Silencing CTNND1 Mediates Triple-Negative Breast Cancer Bone Metastasis via Upregulating CXCR4/CXCL12 Axis and Neutrophils Infiltration in Bone
by Qun Lin, Xiaolin Fang, Gehao Liang, Qing Luo, Yinghuan Cen, Yu Shi, Shijie Jia, Juanmei Li, Wenqian Yang, Andrew J. Sanders, Chang Gong and Wenguo Jiang
Cancers 2021, 13(22), 5703; https://doi.org/10.3390/cancers13225703 - 15 Nov 2021
Cited by 17 | Viewed by 3014
Abstract
Bone metastasis from triple-negative breast cancer (TNBC) frequently results in poorer prognosis than other types of breast cancer due to the delay in diagnosis and intervention, lack of effective treatments and more skeletal-related complications. In the present study, we identified CTNND1 as a [...] Read more.
Bone metastasis from triple-negative breast cancer (TNBC) frequently results in poorer prognosis than other types of breast cancer due to the delay in diagnosis and intervention, lack of effective treatments and more skeletal-related complications. In the present study, we identified CTNND1 as a most reduced molecule in metastatic bone lesion from TNBC by way of high throughput sequencing of TNBC samples. In vivo experiments revealed that knockdown of CTNND1 enhanced tumor cells metastasis to bones and also increased neutrophils infiltration in bones. In vitro, we demonstrated that knockdown of CTNND1 accelerated epithelial–mesenchymal transformation (EMT) of tumor cells and their recruitment to bones. The involvement by CTNND1 in EMT and bone homing was achieved by upregulating CXCR4 via activating the PI3K/AKT/HIF-1αpathway. Moreover, TNBC cells with reduced expression of CTNND1 elicited cytotoxic T-cells responses through accelerating neutrophils infiltration by secreting more GM-CSF and IL-8. Clinically, patients with triple-negative breast cancer and lower level of CTNND1 had shorter overall survival (OS) and distant metastasis-free survival (DMFS). It was concluded that downregulation of CTNND1 played a critical role in facilitating bone metastasis of TNBC and that CTNND1 might be a potential biomarker for predicting the risk of bone metastases in TNBC. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules in Metastasis)
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15 pages, 2733 KiB  
Article
E-Cadherin Regulates Mitochondrial Membrane Potential in Cancer Cells
by Hydari Masuma Begum, Chelsea Mariano, Hao Zhou and Keyue Shen
Cancers 2021, 13(20), 5054; https://doi.org/10.3390/cancers13205054 - 9 Oct 2021
Cited by 8 | Viewed by 2199
Abstract
Epithelial cancer cells often have unusually higher mitochondrial membrane potential (ΔΨm) than their normal counterparts, which has been associated with increased invasiveness in vitro and higher metastatic potential in vivo. However, the mechanisms by which ΔΨm in cancer cells is [...] Read more.
Epithelial cancer cells often have unusually higher mitochondrial membrane potential (ΔΨm) than their normal counterparts, which has been associated with increased invasiveness in vitro and higher metastatic potential in vivo. However, the mechanisms by which ΔΨm in cancer cells is regulated in tumor microenvironment (TME) remain unclear. In this study, we used an in vitro micropatterning platform to recapitulate biophysical confinement cues in the TME and investigated the mechanisms by which these regulate cancer cell ΔΨm. We found that micropatterning resulted in a spatial distribution of ΔΨm, which correlated with the level of E-cadherin mediated intercellular adhesion. There was a stark contrast in the spatial distribution of ΔΨm in the micropattern of E-cadherin-negative breast cancer cells (MDA-MB-231) compared to that of the high E-cadherin expressing (MCF-7) cancer cells. Disruption and knockout of E-cadherin adhesions rescued the low ΔΨm found at the center of MCF-7 micropatterns with high E-cadherin expression, while E-cadherin overexpression in MDA-MB-231 and MCF-7 cells lowered their ΔΨm at the micropattern center. These results show that E-cadherin plays an important role in regulating the ΔΨm of cancer cells in the context of biophysical cues in TME. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules in Metastasis)
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20 pages, 6074 KiB  
Article
SIPA1 Is a Modulator of HGF/MET Induced Tumour Metastasis via the Regulation of Tight Junction-Based Cell to Cell Barrier Function
by Chang Liu, Wenguo Jiang, Lijian Zhang, Rachel Hargest and Tracey A. Martin
Cancers 2021, 13(7), 1747; https://doi.org/10.3390/cancers13071747 - 6 Apr 2021
Cited by 4 | Viewed by 2886
Abstract
Background: Lung cancer is the leading cause of cancer death. SIPA1 is a mitogen induced GTPase activating protein (GAP) and may hamper cell cycle progression. SIPA1 has been shown to be involved in MET signaling and may contribute to tight junction (TJ) function [...] Read more.
Background: Lung cancer is the leading cause of cancer death. SIPA1 is a mitogen induced GTPase activating protein (GAP) and may hamper cell cycle progression. SIPA1 has been shown to be involved in MET signaling and may contribute to tight junction (TJ) function and cancer metastasis. Methods: Human lung tumour cohorts were analyzed. In vitro cell function assays were performed after knock down of SIPA1 in lung cancer cells with/without treatment. Quantitative polymerase chain reaction (qPCR) and western blotting were performed to analyze expression of HGF (hepatocyte growth factor), MET, and their downstream markers. Immunohistochemistry (IHC) and immunofluorescence (IFC) staining were performed. Results: Higher expression of SIPA1 in lung tumours was associated with a poorer prognosis. Knockdown of SIPA1 decreased invasiveness and proliferation of in vitro cell lines, and the SIPA1 knockdown cells demonstrated leaky barriers. Knockdown of SIPA1 decreased tight junction-based barrier function by downregulating MET at the protein but not the transcript level, through silencing of Grb2, SOCS, and PKCμ (Protein kinase Cµ), reducing the internalization and recycling of MET. Elevated levels of SIPA1 protein are correlated with receptor tyrosine kinases (RTKs), especially HGF/MET and TJs. The regulation of HGF on barrier function and invasion required the presence of SIPA1. Conclusions: SIPA1 plays an essential role in lung tumourigenesis and metastasis. SIPA1 may be a diagnostic and prognostic predictive biomarker. SIPA1 may also be a potential therapeutic target for non-small cell lung cancer (NSCLC) patients with aberrant MET expression and drug resistance. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules in Metastasis)
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Review

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17 pages, 1290 KiB  
Review
Claudins and Gastric Cancer: An Overview
by Itaru Hashimoto and Takashi Oshima
Cancers 2022, 14(2), 290; https://doi.org/10.3390/cancers14020290 - 7 Jan 2022
Cited by 51 | Viewed by 9453
Abstract
Despite recent improvements in diagnostic ability and treatment strategies, advanced gastric cancer (GC) has a high frequency of recurrence and metastasis, with poor prognosis. To improve the treatment results of GC, the search for new treatment targets from proteins related to epithelial–mesenchymal transition [...] Read more.
Despite recent improvements in diagnostic ability and treatment strategies, advanced gastric cancer (GC) has a high frequency of recurrence and metastasis, with poor prognosis. To improve the treatment results of GC, the search for new treatment targets from proteins related to epithelial–mesenchymal transition (EMT) and cell–cell adhesion is currently being conducted. EMT plays an important role in cancer metastasis and is initiated by the loss of cell–cell adhesion, such as tight junctions (TJs), adherens junctions, desmosomes, and gap junctions. Among these, claudins (CLDNs) are highly expressed in some cancers, including GC. Abnormal expression of CLDN1, CLDN2, CLDN3, CLDN4, CLDN6, CLDN7, CLDN10, CLDN11, CLDN14, CLDN17, CLDN18, and CLDN23 have been reported. Among these, CLDN18 is of particular interest. In The Cancer Genome Atlas, GC was classified into four new molecular subtypes, and CLDN18–ARHGAP fusion was observed in the genomically stable type. An anti-CLDN18.2 antibody drug was recently developed as a therapeutic drug for GC, and the results of clinical trials are highly predictable. Thus, CLDNs are highly expressed in GC as TJs and are expected targets for new antibody drugs. Herein, we review the literature on CLDNs, focusing on CLDN18 in GC. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules in Metastasis)
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17 pages, 1741 KiB  
Review
The Autophagic Route of E-Cadherin and Cell Adhesion Molecules in Cancer Progression
by Manuela Santarosa and Roberta Maestro
Cancers 2021, 13(24), 6328; https://doi.org/10.3390/cancers13246328 - 16 Dec 2021
Cited by 12 | Viewed by 3921
Abstract
Cell-to-cell adhesion is a key element in epithelial tissue integrity and homeostasis during embryogenesis, response to damage, and differentiation. Loss of cell adhesion and gain of mesenchymal features, a phenomenon known as epithelial to mesenchymal transition (EMT), are essential steps in cancer progression. [...] Read more.
Cell-to-cell adhesion is a key element in epithelial tissue integrity and homeostasis during embryogenesis, response to damage, and differentiation. Loss of cell adhesion and gain of mesenchymal features, a phenomenon known as epithelial to mesenchymal transition (EMT), are essential steps in cancer progression. Interestingly, downregulation or degradation by endocytosis of epithelial adhesion molecules (e.g., E-cadherin) associates with EMT and promotes cell migration. Autophagy is a physiological intracellular degradation and recycling process. In cancer, it is thought to exert a tumor suppressive role in the early phases of cell transformation but, once cells have gained a fully transformed phenotype, autophagy may fuel malignant progression by promoting EMT and conferring drug resistance. In this review, we discuss the crosstalk between autophagy, EMT, and turnover of epithelial cell adhesion molecules, with particular attention to E-cadherin. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules in Metastasis)
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28 pages, 1681 KiB  
Review
The Clinical and Theranostic Values of Activated Leukocyte Cell Adhesion Molecule (ALCAM)/CD166 in Human Solid Cancers
by Yiming Yang, Andrew J. Sanders, Q. Ping Dou, David G. Jiang, Amber Xinyu Li and Wen G. Jiang
Cancers 2021, 13(20), 5187; https://doi.org/10.3390/cancers13205187 - 15 Oct 2021
Cited by 10 | Viewed by 2666
Abstract
Activated leukocyte cell adhesion molecule (ALCAM), also known as CD166, is a cell adhesion protein that is found in multiple cell types. ALCAM has multiple and diverse roles in various physiological and pathological conditions, including inflammation and cancer. There has been compelling evidence [...] Read more.
Activated leukocyte cell adhesion molecule (ALCAM), also known as CD166, is a cell adhesion protein that is found in multiple cell types. ALCAM has multiple and diverse roles in various physiological and pathological conditions, including inflammation and cancer. There has been compelling evidence of ALCAM’s prognostic value in solid cancers, indicating that it is a potential therapeutic target. The present article overviews the recent findings and progress in ALCAM and its involvement in cancer, with a primary focus on its clinical connections in cancer and therapeutic values. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules in Metastasis)
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19 pages, 1599 KiB  
Review
Roles of the HOX Proteins in Cancer Invasion and Metastasis
by Ana Paço, Simone Aparecida de Bessa Garcia, Joana Leitão Castro, Ana Rita Costa-Pinto and Renata Freitas
Cancers 2021, 13(1), 10; https://doi.org/10.3390/cancers13010010 - 22 Dec 2020
Cited by 30 | Viewed by 4039
Abstract
Invasion and metastasis correspond to the foremost cause of cancer-related death, and the molecular networks behind these two processes are extremely complex and dependent on the intra- and extracellular conditions along with the prime of the premetastatic niche. Currently, several studies suggest an [...] Read more.
Invasion and metastasis correspond to the foremost cause of cancer-related death, and the molecular networks behind these two processes are extremely complex and dependent on the intra- and extracellular conditions along with the prime of the premetastatic niche. Currently, several studies suggest an association between the levels of HOX genes expression and cancer cell invasion and metastasis, which favour the formation of novel tumour masses. The deregulation of HOX genes by HMGA2/TET1 signalling and the regulatory effect of noncoding RNAs generated by the HOX loci can also promote invasion and metastasis, interfering with the expression of HOX genes or other genes relevant to these processes. In this review, we present five molecular mechanisms of HOX deregulation by which the HOX clusters products may affect invasion and metastatic processes in solid tumours. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules in Metastasis)
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