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Tumor Cell Invasion and Metastases

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2019) | Viewed by 71380

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Prof. Dr. Giovanni Barillari

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Department of Clinical Sciences and Translational Medicine, University “Tor Vergata”, 00161 Rome, Italy
Interests: tumor cell invasion and metastases; endothelial cell invasion and tumor-associated new vessel formation; tumor diagnostic/prognostic markers; anti-tumor drugs
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Dear Colleagues,

I wish to underscore that the vast majority of cancer-related deaths are attributable to metastasis, the process by which malignant cells detach from the primary tumor and diffuse throughout the organism, giving rise to secondary tumors. In fact, in contrast to primary tumors, metastases are scarcely treatable with surgery and/or chemotherapy.

Metastasis is accomplished through sequential steps, whereby malignant cells: 1) invade surrounding matrices and cell layers; 2) penetrate into neighboring blood/lymphatic vessels, and are transported through the vasculature; 3) arrest, exit from vessels, and localize into different organs; 4) adapt, survive, and then proliferate in the foreign microenvironments.

These events, which depend on cancer cells’ striking migratory and adaptive capabilities, are governed by genetic/epigenetic changes within the tumor cells, and are favored by non-neoplastic stromal cells.

However, in order to become established, metastases require the formation of new blood vessels sustaining the growing need for oxygen and nutrients, and have to evade host immune defenses.

This Special Issue will focus on the cellular and molecular pathways leading to metastasis or counteracting its onset. Essentially, the issue is aimed at either stimulating novel investigations or summarizing recent literature on this important theme.

Prof. Dr. Giovanni Barillari
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.

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Keywords

cancer metastasis
tumor cell invasion
circulating cancer cells
cancer stem cells
metastatic supportive niche
tumor cell survival
metastases and inflammation
metastases therapeutic targets

Related Special Issue

Cancer Cell Invasion and Metastases 2.0 in International Journal of Molecular Sciences (13 articles)

Published Papers (12 papers)

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Research

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18 pages, 7795 KiB

Open AccessArticle

Microcalcifications Drive Breast Cancer Occurrence and Development by Macrophage-Mediated Epithelial to Mesenchymal Transition

by Manuel Scimeca, Rita Bonfiglio, Erika Menichini, Loredana Albonici, Nicoletta Urbano, Maria Teresa De Caro, Alessandro Mauriello, Orazio Schillaci, Alessandra Gambacurta and Elena Bonanno

Int. J. Mol. Sci. 2019, 20(22), 5633; https://doi.org/10.3390/ijms20225633 - 11 Nov 2019

Cited by 32 | Viewed by 4663

Abstract

Background: This study aims to investigate: (a) the putative association between the presence of microcalcifications and the expression of both epithelial-to-mesenchymal transition and bone biomarkers, (b) the role of microcalcifications in the breast osteoblast-like cells (BOLCs) formation, and (c) the association between microcalcification composition and breast cancer progression. Methods: We collected 174 biopsies on which we performed immunohistochemical and ultrastructural analysis. In vitro experiments were performed to demonstrate the relationship among microcalcification, BOLCs development, and breast cancer occurrence. Ex vivo investigations demonstrated the significant increase of breast osteoblast-like cells in breast lesions with microcalcifications with respect to those without microcalcifications. Results: In vitro data displayed that in the presence of calcium oxalate and activated monocytes, breast cancer cells undergo epithelial to mesenchymal transition. Also, in this condition, cells acquired an osteoblast phenotype, thus producing hydroxyapatite. To further confirm in vitro data, we studied 15 benign lesions with microcalcification from patients that developed a malignant condition in the same breast quadrant. Immunohistochemical analysis showed macrophages’ polarization in benign lesions with calcium oxalate. Conclusions: Altogether, our data shed new light about the role of microcalcifications in breast cancer occurrence and progression. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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15 pages, 10805 KiB

Open AccessArticle

HMGA2 Contributes to Distant Metastasis and Poor Prognosis by Promoting Angiogenesis in Oral Squamous Cell Carcinoma

by Junki Sakata, Akiyuki Hirosue, Ryoji Yoshida, Kenta Kawahara, Yuichiro Matsuoka, Tatsuro Yamamoto, Masafumi Nakamoto, Masatoshi Hirayama, Nozomu Takahashi, Takuya Nakamura, Hidetaka Arita, Hikaru Nakashima, Masashi Nagata, Akimitsu Hiraki, Masanori Shinohara and Hideki Nakayama

Int. J. Mol. Sci. 2019, 20(10), 2473; https://doi.org/10.3390/ijms20102473 - 19 May 2019

Cited by 27 | Viewed by 3701

Abstract

The highly malignant phenotype of oral squamous cell carcinoma (OSCC), including the presence of nodal and distant metastasis, reduces patient survival. High-mobility group A protein 2 (HMGA2) is a non-histone chromatin factor that is involved in advanced malignant phenotypes and poor prognosis in several human cancers. However, its biological role in OSCC remains to be elucidated. The purpose of this study was to determine the clinical significance and role of HMGA2 in the malignant potential of OSCC. We first investigated the expression pattern of HMGA2 and its clinical relevance in 110 OSCC specimens using immunohistochemical staining. In addition, we examined the effects HMGA2 on the regulation of vascular endothelial growth factor (VEGF)-A, VEGF-C, and fibroblast growth factor (FGF)-2, which are related to angiogenesis, in vitro. High expression of HMGA2 was significantly correlated with distant metastasis and poor prognosis. Further, HMGA2 depletion in OSCC cells reduced the expression of angiogenesis genes. In OSCC tissues with high HMGA2 expression, angiogenesis genes were increased and a high proportion of blood vessels was observed. These findings suggest that HMGA2 plays a significant role in the regulation of angiogenesis and might be a potential biomarker to predict distant metastasis and prognosis in OSCC. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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20 pages, 4291 KiB

Open AccessArticle

PMN-MDSCs Enhance CTC Metastatic Properties through Reciprocal Interactions via ROS/Notch/Nodal Signaling

by Marc L. Sprouse, Thomas Welte, Debasish Boral, Haowen N. Liu, Wei Yin, Monika Vishnoi, Debalina Goswami-Sewell, Lili Li, Guangsheng Pei, Peilin Jia, Isabella C. Glitza-Oliva and Dario Marchetti

Int. J. Mol. Sci. 2019, 20(8), 1916; https://doi.org/10.3390/ijms20081916 - 18 Apr 2019

Cited by 103 | Viewed by 9146

Abstract

Intratumoral infiltration of myeloid-derived suppressor cells (MDSCs) is known to promote neoplastic growth by inhibiting the tumoricidal activity of T cells. However, direct interactions between patient-derived MDSCs and circulating tumors cells (CTCs) within the microenvironment of blood remain unexplored. Dissecting interplays between CTCs and circulatory MDSCs by heterotypic CTC/MDSC clustering is critical as a key mechanism to promote CTC survival and sustain the metastatic process. We characterized CTCs and polymorphonuclear-MDSCs (PMN-MDSCs) isolated in parallel from peripheral blood of metastatic melanoma and breast cancer patients by multi-parametric flow cytometry. Transplantation of both cell populations in the systemic circulation of mice revealed significantly enhanced dissemination and metastasis in mice co-injected with CTCs and PMN-MDSCs compared to mice injected with CTCs or MDSCs alone. Notably, CTC/PMN-MDSC clusters were detected in vitro and in vivo either in patients’ blood or by longitudinal monitoring of blood from animals. This was coupled with in vitro co-culturing of cell populations, demonstrating that CTCs formed physical clusters with PMN-MDSCs; and induced their pro-tumorigenic differentiation through paracrine Nodal signaling, augmenting the production of reactive oxygen species (ROS) by PMN-MDSCs. These findings were validated by detecting significantly higher Nodal and ROS levels in blood of cancer patients in the presence of naïve, heterotypic CTC/PMN-MDSC clusters. Augmented PMN-MDSC ROS upregulated Notch1 receptor expression in CTCs through the ROS-NRF2-ARE axis, thus priming CTCs to respond to ligand-mediated (Jagged1) Notch activation. Jagged1-expressing PMN-MDSCs contributed to enhanced Notch activation in CTCs by engagement of Notch1 receptor. The reciprocity of CTC/PMN-MDSC bi-directional paracrine interactions and signaling was functionally validated in inhibitor-based analyses, demonstrating that combined Nodal and ROS inhibition abrogated CTC/PMN-MDSC interactions and led to a reduction of CTC survival and proliferation. This study provides seminal evidence showing that PMN-MDSCs, additive to their immuno-suppressive roles, directly interact with CTCs and promote their dissemination and metastatic potency. Targeting CTC/PMN-MDSC heterotypic clusters and associated crosstalks can therefore represent a novel therapeutic avenue for limiting hematogenous spread of metastatic disease. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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Review

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29 pages, 703 KiB

Open AccessReview

The Impact of Matrix Metalloproteinase-9 on the Sequential Steps of the Metastatic Process

by Giovanni Barillari

Int. J. Mol. Sci. 2020, 21(12), 4526; https://doi.org/10.3390/ijms21124526 - 25 Jun 2020

Cited by 49 | Viewed by 4446

Abstract

In industrialized countries, cancer is the second leading cause of death after cardiovascular disease. Most cancer patients die because of metastases, which consist of the self-transplantation of malignant cells in anatomical sites other than the one from where the tumor arose. Disseminated cancer cells retain the phenotypic features of the primary tumor, and display very poor differentiation indices and functional regulation. Upon arrival at the target organ, they replace preexisting, normal cells, thereby permanently compromising the patient’s health; the metastasis can, in turn, metastasize. The spread of cancer cells implies the degradation of the extracellular matrix by a variety of enzymes, among which the matrix metalloproteinase (MMP)-9 is particularly effective. This article reviews the available published literature concerning the important role that MMP-9 has in the metastatic process. Additionally, information is provided on therapeutic approaches aimed at counteracting, or even preventing, the development of metastasis via the use of MMP-9 antagonists. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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53 pages, 1239 KiB

Open AccessReview

Role of VEGFs/VEGFR-1 Signaling and Its Inhibition in Modulating Tumor Invasion: Experimental Evidence in Different Metastatic Cancer Models

by Claudia Ceci, Maria Grazia Atzori, Pedro Miguel Lacal and Grazia Graziani

Int. J. Mol. Sci. 2020, 21(4), 1388; https://doi.org/10.3390/ijms21041388 - 18 Feb 2020

Cited by 119 | Viewed by 9148

Abstract

The vascular endothelial growth factor (VEGF) family members, VEGF-A, placenta growth factor (PlGF), and to a lesser extent VEGF-B, play an essential role in tumor-associated angiogenesis, tissue infiltration, and metastasis formation. Although VEGF-A can activate both VEGFR-1 and VEGFR-2 membrane receptors, PlGF and VEGF-B exclusively interact with VEGFR-1. Differently from VEGFR-2, which is involved both in physiological and pathological angiogenesis, in the adult VEGFR-1 is required only for pathological angiogenesis. Besides this role in tumor endothelium, ligand-mediated stimulation of VEGFR-1 expressed in tumor cells may directly induce cell chemotaxis and extracellular matrix invasion. Furthermore, VEGFR-1 activation in myeloid progenitors and tumor-associated macrophages favors cancer immune escape through the release of immunosuppressive cytokines. These properties have prompted a number of preclinical and clinical studies to analyze VEGFR-1 involvement in the metastatic process. The aim of the present review is to highlight the contribution of VEGFs/VEGFR-1 signaling in the progression of different tumor types and to provide an overview of the therapeutic approaches targeting VEGFR-1 currently under investigation. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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17 pages, 11335 KiB

Open AccessReview

Conjunctival Melanoma: Genetic and Epigenetic Insights of a Distinct Type of Melanoma

by Ernesto Rossi, Giovanni Schinzari, Brigida Anna Maiorano, Monica Maria Pagliara, Alessandro Di Stefani, Emilio Bria, Ketty Peris, Maria Antonietta Blasi and Giampaolo Tortora

Int. J. Mol. Sci. 2019, 20(21), 5447; https://doi.org/10.3390/ijms20215447 - 31 Oct 2019

Cited by 24 | Viewed by 3913

Abstract

Conjunctival melanoma (CjM) is a rare, primary cancer of the ocular region. Genetic and epigenetic characteristics of conjunctival melanoma have not been completely elucidated yet. Conjunctival melanoma presents similarities with cutaneous melanoma, with substantial differences in the biological behavior. We reviewed the genetic and epigenetic insights of CjM involved in invasion and metastatic spread. CjM is commonly characterized by mutations of v-raf murine sarcoma viral oncogene homolog B1 (BRAF), neurofibromin 1 (NF1) and telomerase reverse transcriptase (TERT), high expression of mammalian target of rapamycin (mTOR) and heat shock protein 90 (HSP90), frequent phosphatase and tensin homolog (PTEN) loss and upregulation of specific miRNAs. These features should identify CjM as a distinct subset of melanoma with its own profile, which is more similar to cutaneous melanoma than mucosal melanoma and remarkably different from uveal melanoma. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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18 pages, 937 KiB

Open AccessReview

The Janus Face of Tumor Microenvironment Targeted by Immunotherapy

by Maria Buoncervello, Lucia Gabriele and Elena Toschi

Int. J. Mol. Sci. 2019, 20(17), 4320; https://doi.org/10.3390/ijms20174320 - 03 Sep 2019

Cited by 36 | Viewed by 4712

Abstract

The tumor microenvironment (TME) is a complex entity where host immune and non-immune cells establish a dynamic crosstalk with cancer cells. Through cell-cell interactions, which are mediated by key signals, such as the PD-1/PD-L1 axis, as well as the release of soluble mediators, this articulated process defines the nature of TME determining tumor development, prognosis, and response to therapy. Specifically, tumors are characterized by cellular plasticity that allows for the microenvironment to polarize towards inflammation or immunosuppression. Thus, the dynamic crosstalk among cancer, stromal, and immune components crucially favors the dominance of one of the Janus-faced contexture of TME crucial to the outcome of tumor development and therapeutic response. However, mostly, TME is dominated by an immunosuppressive landscape that blocks antitumor immunity and sustain tumor progression. Hence, in most cases, the immunosuppressive components of TME are highly competent in suppressing tumor-specific CD8⁺ T lymphocytes, the effectors of cancer destruction. In this complex context, immunotherapy aims to arm the hidden Janus face of TME disclosing and potentiating antitumor immune signals. Herein, we discuss recent knowledge on the immunosuppressive crosstalk within TME, and share perspectives on how immunotherapeutic approaches may exploit tumor immune signals to generate antitumor immunity. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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20 pages, 1574 KiB

Open AccessReview

The Role of SATB1 in Tumour Progression and Metastasis

by Natalia Glatzel-Plucińska, Aleksandra Piotrowska, Piotr Dzięgiel and Marzenna Podhorska-Okołów

Int. J. Mol. Sci. 2019, 20(17), 4156; https://doi.org/10.3390/ijms20174156 - 25 Aug 2019

Cited by 29 | Viewed by 4452

Abstract

Carcinogenesis is a long-drawn, multistep process, in which metastatic spread is an unequivocal hallmark of a poor prognosis. The progression and dissemination of epithelial cancers is commonly thought to rely on the epidermal-mesenchymal transition (EMT) process. During EMT, epithelial cells lose their junctions and apical-basal polarity, and they acquire a mesenchymal phenotype with its migratory and invasive capabilities. One of the proteins involved in cancer progression and EMT may be SATB1 (Special AT-Rich Binding Protein 1)—a chromatin organiser and a global transcriptional regulator. SATB1 organizes chromatin into spatial loops, providing a “docking site” necessary for the binding of further transcription factors and chromatin modifying enzymes. SATB1 has the ability to regulate whole sets of genes, even those located on distant chromosomes. SATB1 was found to be overexpressed in numerous malignancies, including lymphomas, breast, colorectal, prostate, liver, bladder and ovarian cancers. In the solid tumours, an elevated SATB1 level was observed to be associated with an aggressive phenotype, presence of lymph node, distant metastases, and a poor prognosis. In this review, we briefly describe the prognostic significance of SATB1 expression in most common human cancers, and analyse its impact on EMT and metastasis. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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20 pages, 940 KiB

Open AccessReview

Adipose-Derived Stem Cells in Cancer Progression: New Perspectives and Opportunities

by Maria Giovanna Scioli, Gabriele Storti, Federico D’Amico, Pietro Gentile, Bong-Sung Kim, Valerio Cervelli and Augusto Orlandi

Int. J. Mol. Sci. 2019, 20(13), 3296; https://doi.org/10.3390/ijms20133296 - 04 Jul 2019

Cited by 49 | Viewed by 4806

Abstract

Growing importance has been attributed to interactions between tumors, the stromal microenvironment and adult mesenchymal stem cells. Adipose-derived stem cells (ASCs) are routinely employed in regenerative medicine and in autologous fat transfer procedures. To date, clinical trials have failed to demonstrate the potential pro-oncogenic role of ASC enrichment. Nevertheless, some pre-clinical studies from in vitro and in vivo models have suggested that ASCs act as a potential tumor promoter for different cancer cell types, and support tumor progression and invasiveness through the activation of several intracellular signals. Interaction with the tumor microenvironment and extracellular matrix remodeling, the exosomal release of pro-oncogenic factors as well as the induction of epithelial-mesenchymal transitions are the most investigated mechanisms. Moreover, ASCs have also demonstrated an elective tumor homing capacity and this tumor-targeting capacity makes them a suitable carrier for anti-cancer drug delivery. New genetic and applied nanotechnologies may help to design promising anti-cancer cell-based approaches through the release of loaded intracellular nanoparticles. These new anti-cancer therapies can more effectively target tumor cells, reaching higher local concentrations even in pharmacological sanctuaries, and thus minimizing systemic adverse drug effects. The potential interplay between ASCs and tumors and potential ASCs-based therapeutic approaches are discussed. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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15 pages, 651 KiB

Open AccessReview

Cutaneous Metastasis after Surgery, Injury, Lymphadenopathy, and Peritonitis: Possible Mechanisms

by Isao Otsuka

Int. J. Mol. Sci. 2019, 20(13), 3286; https://doi.org/10.3390/ijms20133286 - 04 Jul 2019

Cited by 13 | Viewed by 5843

Abstract

Cutaneous metastases from internal malignancies are uncommon. Umbilical metastasis, also known as Sister Joseph nodule (SJN), develops in patients with carcinomatous peritonitis or superficial lymphadenopathy, while non-SJN skin metastases develop after surgery, injury, and lymphadenopathy. In this review, the possible mechanisms of skin metastases are discussed. SJNs develop by the contiguous or lymphatic spread of tumor cells. After surgery and injury, tumor cells spread by direct implantation or hematogenous metastasis, and after lymphadenopathy, they spread by extranodal extension. The inflammatory response occurring during wound healing is exploited by tumor cells and facilitates tumor growth. Macrophages are crucial drivers of tumor-promoting inflammation, which is a source of survival, growth and angiogenic factors. Angiogenesis is promoted by the vascular endothelial growth factor (VEGF), which also mediates tumor-associated immunodeficiency. In the subcutaneous tissues that surround metastatic lymph nodes, adipocytes promote tumor growth. In the elderly, age-associated immunosuppression may facilitate hematogenous metastasis. Anti-VEGF therapy affects recurrence patterns but at the same time, may increase the risk of skin metastases. Immune suppression associated with inflammation may play a key role in skin metastasis development. Thus, immune therapies, including immune checkpoint inhibitors reactivating cytotoxic T-cell function and inhibiting tumor-associated macrophage function, appear promising. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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32 pages, 2654 KiB

Open AccessReview

Multifaceted Role of the Placental Growth Factor (PlGF) in the Antitumor Immune Response and Cancer Progression

by Loredana Albonici, Maria Gabriella Giganti, Andrea Modesti, Vittorio Manzari and Roberto Bei

Int. J. Mol. Sci. 2019, 20(12), 2970; https://doi.org/10.3390/ijms20122970 - 18 Jun 2019

Cited by 54 | Viewed by 8529

Abstract

The sharing of molecules function that affects both tumor growth and neoangiogenesis with cells of the immune system creates a mutual interplay that impairs the host’s immune response against tumor progression. Increasing evidence shows that tumors are able to create an immunosuppressive microenvironment by recruiting specific immune cells. Moreover, molecules produced by tumor and inflammatory cells in the tumor microenvironment create an immunosuppressive milieu able to inhibit the development of an efficient immune response against cancer cells and thus fostering tumor growth and progression. In addition, the immunoediting could select cancer cells that are less immunogenic or more resistant to lysis. In this review, we summarize recent findings regarding the immunomodulatory effects and cancer progression of the angiogenic growth factor namely placental growth factor (PlGF) and address the biological complex effects of this cytokine. Different pathways of the innate and adaptive immune response in which, directly or indirectly, PlGF is involved in promoting tumor immune escape and metastasis will be described. PlGF is important for building up vascular structures and functions. Although PlGF effects on vascular and tumor growth have been widely summarized, its functions in modulating the immune intra-tumoral microenvironment have been less highlighted. In agreement with PlGF functions, different antitumor strategies can be envisioned. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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17 pages, 18303 KiB

Open AccessReview

Involvement of Extracellular Vesicles in Vascular-Related Functions in Cancer Progression and Metastasis

by Shinsuke Kikuchi, Yusuke Yoshioka, Marta Prieto-Vila and Takahiro Ochiya

Int. J. Mol. Sci. 2019, 20(10), 2584; https://doi.org/10.3390/ijms20102584 - 26 May 2019

Cited by 48 | Viewed by 7240

Abstract

The primary cause of mortality among patients with cancer is the progression of the tumor, better known as cancer invasion and metastasis. Cancer progression involves a series of biologically important steps in which the cross-talk between cancer cells and the cells in the surrounding environment is positioned as an important issue. Notably, angiogenesis is a key tumorigenic phenomenon for cancer progression. Cancer-related extracellular vesicles (EVs) commonly contribute to the modulation of a microenvironment favorable to cancer cells through their function of cell-to-cell communication. Vascular-related cells such as endothelial cells (ECs) and platelets activated by cancer cells and cancer-derived EVs develop procoagulant and proinflammatory statuses, which help excite the tumor environment, and play major roles in tumor progression, including in tumor extravasation, tumor cell microthrombi formation, platelet aggregation, and metastasis. In particular, cancer-derived EVs influence ECs, which then play multiple roles such as contributing to tumor angiogenesis, loss of endothelial vascular barrier by binding to ECs, and the subsequent endothelial-to-mesenchymal transition, i.e., extracellular matrix remodeling. Thus, cell-to-cell communication between cancer cells and ECs via EVs may be an important target for controlling cancer progression. This review describes the current knowledge regarding the involvement of EVs, especially exosomes derived from cancer cells, in EC-related cancer progression. Full article

(This article belongs to the Special Issue Tumor Cell Invasion and Metastases)

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