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IJMS
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Cancer Cell Invasion and Metastases 3.0
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Cancer Cell Invasion and Metastases 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 5954

Special Issue Editors

Prof. Dr. Giovanni Barillari

E-Mail Website
Guest Editor
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
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Roberto Bei

E-Mail Website
Guest Editor
Department of Clinical Sciences and Translational Medicine, University of Rome “Tor Vergata”, 00133 Rome, Italy
Interests: cancer immunotherapy; natural compounds and cancer; cancer vaccines; cancer prevention and treatment in preclinical models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce the reopening of the Special Issue in IJMS, entitled “Cancer Cell Invasion and Metastases”.

Twenty-four articles were published in the first and second volumes of the Special Issue: they described the cross-talk among cancer, stromal and immune cells that lead to tumor cell invasion and spreading, cancer immune escape and the onset of metastasis, the role of extracellular vesicles, hormones or inflammation in cancerogenesis, the signaling pathways or non-coding RNAs involved in tumor cell differentiation or invasiveness, and the biomarkers of tumor progression.

In the third part of the Special Issue, we invite you to continue the path already undertaken by sending research papers or reviews dealing with cellular events and molecular pathways leading to cancer metastasis, including cellular stemness, epithelial–mesenchymal transition, extracellular matrix remodeling, adhesion receptors and proteolytic enzymes, growth/chemotactic factors, or inflammatory cytokines/chemokines. Studies concerning possible inhibitors of the above-mentioned phenomena or molecules will be very welcome.

We strongly hope that, as for the first and second volume of the Special Issue, the third one will provide useful information to understand and counter cancer metastatic process.

Prof. Dr. Giovanni Barillari
Prof. Dr. Roberto Bei
Guest Editors

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

  • cancer metastasis
  • tumor cell invasion
  • epithelial–mesenchymal transition
  • circulating cancer cells
  • cancer stem cells
  • metastatic supportive niche
  • tumor cell survival
  • metastases and inflammation
  • metastases and immune response
  • cancer-related extracellular vesicles
  • non-coding RNAs and cancer
  • metastases therapeutic targets

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Published Papers (3 papers)

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Research

17 pages, 7257 KiB  
Article
Long Noncoding RNA ZBED5-AS1 Facilitates Tumor Progression and Metastasis in Lung Adenocarcinoma via ZNF146/ATR/Chk1 Axis
by Feng Jiang, Xiaolu Huang, Liqun Ling, Shiyi Tang, Huixin Zhou, Xueding Cai and Yumin Wang
Int. J. Mol. Sci. 2023, 24(18), 13925; https://doi.org/10.3390/ijms241813925 - 10 Sep 2023
Cited by 1 | Viewed by 1349
Abstract
Long noncoding RNAs (lncRNAs) have been implicated in tumorigenesis, including lung adenocarcinoma (LUAD). However, the functional and regulatory mechanisms of lncRNAs in LUAD remain poorly understood. In this study, we investigated the role of lncRNA ZBED5-AS1 in LUAD. We found that ZBED5-AS1 was [...] Read more.
Long noncoding RNAs (lncRNAs) have been implicated in tumorigenesis, including lung adenocarcinoma (LUAD). However, the functional and regulatory mechanisms of lncRNAs in LUAD remain poorly understood. In this study, we investigated the role of lncRNA ZBED5-AS1 in LUAD. We found that ZBED5-AS1 was upregulated in LUAD specimens and overexpressed in LUAD cell lines. ZBED5-AS1 promoted LUAD cell proliferation, migration, and invasion in vitro and promoted LUAD cell growth in vivo. ZBED5-AS1 promoted ZNF146 expression, activating the ATR/Chk1 pathway and leading to LUAD progression. We observed that exosomes from LUAD cells have a higher expression of ZBED5-AS1 compared with exosomes from the normal cell line BEAS-2B. Coculture experiments with exosomes showed that ZBED5-AS1 expression was downregulated after coculture with Si-ZBED5-AS1 exosomes, and coculture with exosomes with low ZBED5-AS1 expression inhibited proliferation and invasion of LUAD cells. Our results indicate that ZBED5-AS1 functions as an oncogenic factor in LUAD cells by targeting the ZNF146/ATR/Chk1 axis. Full article
(This article belongs to the Special Issue Cancer Cell Invasion and Metastases 3.0)
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9 pages, 2758 KiB  
Communication
Fate of Entosis: From the Beginning to the End in Untreated Advanced Breast Cancer
by Ireneusz Dziuba, Agata M. Gawel, Paweł Tyrna, Jolanta Rybczynska, Lukasz P. Bialy and Izabela Mlynarczuk-Bialy
Int. J. Mol. Sci. 2023, 24(15), 12142; https://doi.org/10.3390/ijms241512142 - 29 Jul 2023
Cited by 2 | Viewed by 1976
Abstract
Homotypic entosis is a phenomenon in which one cancer cell invades a neighboring cancer cell and is closed entirely within its entotic vacuole. The fate of entosis can lead to inner cell death or survival. Recent evidence draws attention to entosis as a [...] Read more.
Homotypic entosis is a phenomenon in which one cancer cell invades a neighboring cancer cell and is closed entirely within its entotic vacuole. The fate of entosis can lead to inner cell death or survival. Recent evidence draws attention to entosis as a novel prognostic marker in breast cancer. Nevertheless, little is known about the quantity and quality of the process of entosis in human cancer specimens. Here, for the first time, we analyze the frequency of entotic figures in a case of NOS (Non-Other Specified) breast cancer with regard to location: the primary tumor, regional lymph node, and distant metastasis. For the identification of entotic figures, cells were stained using hematoxylin/eosin and assessed using criteria proposed by Mackay. The majority of entotic figures (65%) were found in the lymph node, 27% were found in the primary tumor, and 8% were found in the far metastasis. In the far metastases, entotic figures demonstrated an altered, atypic morphology. Interestingly, in all locations, entosis did not show any signs of cell death. Moreover, the slides were stained for E-cadherin or Ki67, and we identified proliferating (Ki67-positive) inner and outer entotic cells. Therefore, we propose additional criteria for the identification of pro-survival entotic structures in diagnostic histopathology. Full article
(This article belongs to the Special Issue Cancer Cell Invasion and Metastases 3.0)
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Graphical abstract

18 pages, 4921 KiB  
Article
VCAN Hypomethylation and Expression as Predictive Biomarkers of Drug Sensitivity in Upper Urinary Tract Urothelial Carcinoma
by Hao-Lun Luo, Yin-Lun Chang, Hui-Ying Liu, Yen-Ting Wu, Ming-Tse Sung, Yu-Li Su, Chun-Chieh Huang, Pei-Chia Wang and Jei-Ming Peng
Int. J. Mol. Sci. 2023, 24(8), 7486; https://doi.org/10.3390/ijms24087486 - 19 Apr 2023
Cited by 4 | Viewed by 2223
Abstract
Versican (VCAN), also known as extracellular matrix proteoglycan 2, has been suggested as a potential biomarker in cancers. Previous research has found that VCAN is highly expressed in bladder cancer. However, its role in predicting outcomes for patients with upper urinary tract urothelial [...] Read more.
Versican (VCAN), also known as extracellular matrix proteoglycan 2, has been suggested as a potential biomarker in cancers. Previous research has found that VCAN is highly expressed in bladder cancer. However, its role in predicting outcomes for patients with upper urinary tract urothelial cancer (UTUC) is not well understood. In this study, we collected tissues from 10 patients with UTUC, including 6 with and 4 without lymphovascular invasion (LVI), a pathological feature that plays a significant role in determining metastasis. Results from RNA sequencing revealed that the most differentially expressed genes were involved in extracellular matrix organization. Using the TCGA database for clinical correlation, VCAN was identified as a target for study. A chromosome methylation assay showed that VCAN was hypomethylated in tumors with LVI. In our patient samples, VCAN expression was also found to be high in UTUC tumors with LVI. In vitro analysis showed that knocking down VCAN inhibited cell migration but not proliferation. A heatmap analysis also confirmed a significant correlation between VCAN and migration genes. Additionally, silencing VCAN increased the effectiveness of cisplatin, gemcitabine and epirubicin, thus providing potential opportunities for clinical application. Full article
(This article belongs to the Special Issue Cancer Cell Invasion and Metastases 3.0)
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