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Special Issue "Molecular Mechanisms in Cancer Metastasis"

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 (31 March 2019).

Special Issue Editor

Dr. Yusuke Oshima
E-Mail Website
Guest Editor
Faculty of Engineering, University of Toyama, 3190 Gofuku, Toyama 930-8555, Japan
Interests: fluorescent imaging; raman spectroscopy; nonlinear microscopy; optical biopsy; cancer metastasis; cancer diagnosis; osteoporosis; cartilage degeneration and regeneration
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer metastasis is the leading cause of death globally. Even if diagnostics in primary cancer is developed, there is an urgent need to understand whether the cancer is localized or has already spread to other organs. The progressive growth of metastases is often resistant to conventional therapies. Understanding the characteristic differences in the aspect of molecular and cellular biology between primary cancer and metastatic lesions is essential for effective cancer treatment. This Special Issue, “Molecular Mechanisms in Cancer Metastasis”, is a part of the Section ‘’Molecular Pathology, Diagnostics, and Therapeutics’’ in IJMS. Our primary goals of cancer research are technical and instrumental development to address molecular mechanisms in cancer metastasis based on genomics, proteomics, and metabolomics in vivo and in vitro, and the establishment of a cancer metastasis model in experimental animals and molecular imaging techniques in cancer cells and their environment including other cells and extracellular matrix. Metastases can be characterized not only by cancer cells but also by environmental factors including immune cells, stroma cells, secretion vesicles, and the extracellular matrix, but to identify and detect cancer diagnostic biomarkers is still challenging. The aim of this Special Issue is to investigate and/or discuss morphological and molecular dynamics in cancer metastasis. We invite authors to submit full-length original articles and review papers for cancer research in both in vitro and in vivo assay of tumor tissues to reveal the metastasis process and to evaluate therapeutic effects of anti-cancer drugs and their drug delivery toward the clinical application of the technique.

Dr. Yusuke Oshima
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 papers will be 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

  • microenviroment
  • extracelluar matrix
  • drug delivery
  • cancer imaging
  • animal models
  • molecular-guided surgery
  • optical biopsy
  • cancer-specific probes

Published Papers (4 papers)

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Research

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Article
Inhibition of Phosphatidylinositol 3-kinase (PI3K) Signaling Synergistically Potentiates Antitumor Efficacy of Paclitaxel and Overcomes Paclitaxel-Mediated Resistance in Cervical Cancer
Int. J. Mol. Sci. 2019, 20(14), 3383; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20143383 - 10 Jul 2019
Cited by 11 | Viewed by 1348
Abstract
Acquired paclitaxel (PTX) resistance limits its effectiveness and results in advanced cancer progression. This review investigated whether the inhibition of phosphatidylinositol 3-kinase (PI3K) signaling overcomes paclitaxel resistance in cervical cancer. It was established paclitaxel-resistant cell lines (PTX-R ME180/PTX-R HeLa) and determined the combination [...] Read more.
Acquired paclitaxel (PTX) resistance limits its effectiveness and results in advanced cancer progression. This review investigated whether the inhibition of phosphatidylinositol 3-kinase (PI3K) signaling overcomes paclitaxel resistance in cervical cancer. It was established paclitaxel-resistant cell lines (PTX-R ME180/PTX-R HeLa) and determined the combination index for paclitaxel and PI3K inhibitors (BYL-719/ LY294002) by tetrazolium dye assay. Flow cytometry was used to detect the cell cycle and apoptosis. Migration and invasion were explored by wound healing and transwell assays. Genes related to multiple pathways were assessed by a western blot. It was found that the PI3K pathway was significantly activated in paclitaxel-resistant HeLa and ME180 cells compared to parental cells. PTX + PI3K inhibitor combined therapy showed a synergistic effect by strengthening paclitaxel-induced S and G2M arrest in PTX-R cell sublines by the inactivation of cyclin A1, cyclin B1, cyclin E, and Cdc2 expression. Moreover, combination therapy significantly enhanced drug sensitivity and apoptosis through the activation of Bax, and cleavage of poly-(ADP-ribose) polymerase compared with paclitaxel alone. In addition, PI3K inhibition also suppressed tumor migration and invasion by targeting β-catenin and matrix metalloproteinase-2/9. The authors suggest that the combination of a PI3K inhibitor with paclitaxel may enhance antitumor activity through a cascade of PI3K signaling events. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Cancer Metastasis)
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Article
Effect of Chemokine (C-C Motif) Ligand 7 (CCL7) and Its Receptor (CCR2) Expression on Colorectal Cancer Behaviors
Int. J. Mol. Sci. 2019, 20(3), 686; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20030686 - 05 Feb 2019
Cited by 6 | Viewed by 1439
Abstract
Colorectal cancer is the source of one of the most common cancer-related deaths worldwide, where the main cause of patient mortality remains metastasis. The aim of this study was to determine the role of CCL7 (chemokine (C-C motif) ligand 7) in tumor progression [...] Read more.
Colorectal cancer is the source of one of the most common cancer-related deaths worldwide, where the main cause of patient mortality remains metastasis. The aim of this study was to determine the role of CCL7 (chemokine (C-C motif) ligand 7) in tumor progression and finding whether it could predict survival of colorectal cancer patients. Initially, our study focused on the crosstalk between mesenchymal stem cells (MSCs) and CT26 colon carcinoma cells and resulted in identifying CCL7 as a chemokine upregulated in CT26 colon cancer cells cocultured with MSCs, compared with CT26 in monoculture in vitro. Moreover, we showed that MSCs enhance CT26 tumor cell proliferation and migration. We analyzed the effect of CCL7 overexpression on tumor progression in a murine CT26 model, where cells overexpressing CCL7 accelerated the early phase of tumor growth and caused higher lung metastasis rates compared with control mice. Microarray analysis revealed that tumors overexpressing CCL7 had lower expression of immunoglobulins produced by B lymphocytes. Additionally, using Jh mutant mice, we confirmed that in the CT26 model, CCL7 has an immunoglobulin-, and thereby, B-cell-dependent effect on metastasis formation. Finally, higher expression of CCL7 receptor CCR2 (C-C chemokine receptor type 2) was associated with shorter overall survival of colorectal cancer patients. Altogether, we showed that CCL7 is essentially involved in the progression of colorectal cancer in a CT26 mouse model and that the expression of its receptor CCR2 could be related to a different outcome pattern of patients with colorectal carcinoma. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Cancer Metastasis)
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Review

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Review
Molecular Mechanisms of Breast Cancer Metastasis to the Lung: Clinical and Experimental Perspectives
Int. J. Mol. Sci. 2019, 20(9), 2272; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20092272 - 08 May 2019
Cited by 37 | Viewed by 3637
Abstract
Breast cancer is the most commonly diagnosed cancer in women worldwide, and >90% of breast cancer-related deaths are associated with metastasis. Breast cancer spreads preferentially to the lung, brain, bone and liver; termed organ tropism. Current treatment methods for metastatic breast cancer have [...] Read more.
Breast cancer is the most commonly diagnosed cancer in women worldwide, and >90% of breast cancer-related deaths are associated with metastasis. Breast cancer spreads preferentially to the lung, brain, bone and liver; termed organ tropism. Current treatment methods for metastatic breast cancer have been ineffective, compounded by the lack of early prognostic/predictive methods to determine which organs are most susceptible to developing metastases. A better understanding of the mechanisms that drive breast cancer metastasis is crucial for identifying novel biomarkers and therapeutic targets. Lung metastasis is of particular concern as it is associated with significant patient morbidity and a mortality rate of 60–70%. This review highlights the current understanding of breast cancer metastasis to the lung, including discussion of potential new treatment approaches for development. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Cancer Metastasis)
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Review
The Contribution of the Immune System in Bone Metastasis Pathogenesis
Int. J. Mol. Sci. 2019, 20(4), 999; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20040999 - 25 Feb 2019
Cited by 28 | Viewed by 3555
Abstract
Bone metastasis is associated with significant morbidity for cancer patients and results in a reduced quality of life. The bone marrow is a fertile soil containing a complex composition of immune cells that may actually provide an immune-privileged niche for disseminated tumor cells [...] Read more.
Bone metastasis is associated with significant morbidity for cancer patients and results in a reduced quality of life. The bone marrow is a fertile soil containing a complex composition of immune cells that may actually provide an immune-privileged niche for disseminated tumor cells to colonize and proliferate. In this unique immune milieu, multiple immune cells including T cells, natural killer cells, macrophages, dendritic cells, myeloid-derived suppressor cells, and neutrophils are involved in the process of bone metastasis. In this review, we will discuss the crosstalk between immune cells in bone microenvironment and their involvement with cancer cell metastasis to the bone. Furthermore, we will highlight the anti-tumoral and pro-tumoral function of each immune cell type that contributes to bone metastasis. We will end with a discussion of current therapeutic strategies aimed at sensitizing immune cells. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Cancer Metastasis)
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