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Cancers
Special Issues
Cellular Communication, Carcinogenesis and Targeted Interventions
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Cellular Communication, Carcinogenesis and Targeted Interventions

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 3959

Special Issue Editors

Prof. Dr. Jean Jiang

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Guest Editor
Department of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX 78229, USA
Interests: gap junctions and hemichannels; connexins; signaling transmission; breast cancer; osteosarcoma; metastasis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Maria Lucia Zaidan Dagli

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Guest Editor
School of Veterinary Medicine and Animal Science, Universidade de São Paulo, São Paulo, SP 05508-900, Brazil
Interests: connexins; cancer therapy; oncology; cancer chemotherapy; cancer biology; liver; cancer animal models
Prof. Dr. Marc Mesnil

E-Mail Website
Guest Editor
CoMeT Laboratory, UR 24344, Université de Poitiers, 86073 Poitiers, France
Interests: gap junctions; connexins; intercellular communication; cancer; glioma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Human and animal organs are composed of different tissues and various cell types. In order to achieve the harmonization of organ and tissue functions, and keep the body healthy, cell communication is of utmost importance. Cells in tissues communicate closely with each other either directly, by contact, or indirectly, by secretion of soluble factors or extracellular vesicles. Intercellular communication by contact is carried out mainly via three types of interactions:  intercellular recognition or adhesion molecules, gap junctions and the very thin cytoplasmic projections called nanotubes. On the other hand, indirect cellular communication is carried out through secreted molecules that are transported from one cell to another by diffusion over short distances (paracrine communication) or long distances by blood flow (endocrine communication). Indirect intercellular communication can also be achieved by transmitting extracellular vesicles (EVs), such as exosomes and microvesicles, which act as transport shuttles, allowing cells to exchange proteins, RNAs (miRNAs, mRNAs) likely to modify the phenotype of the recipient cell. Gap junction intercellular communication capacity (GJICc) and connexin expression were found to be altered in cancer cells in 1966 (Loewenstein and Kanno, 1966) when the studies on the gap junction involvement in carcinogenesis started. The role of different forms of cell communication, such as the extracellular vesicles, in the neoplastic microenvironment is currently being discussed. Cancer is a devastating disease, and new forms of treatment are usually required for many different cancer types. This Special Issue of Cancers aims to present how the different forms of cellular communication may modify carcinogenesis and cancer treatment outcomes. 

Prof. Dr. Jean Jiang
Prof. Dr. Maria Lucia Zaidan Dagli
Prof. Dr. Marc Mesnil
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 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.

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Published Papers (2 papers)

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Research

19 pages, 6932 KiB  
Article
Inhibitory Effects of Alpha-Connexin Carboxyl-Terminal Peptide on Canine Mammary Epithelial Cells: A Study on Benign and Malignant Phenotypes
by Ivone Izabel Mackowiak da Fonseca, Marcia Kazumi Nagamine, Ayami Sato, Carlos Alberto Rossatto-Jr, Elizabeth Shinmay Yeh and Maria Lucia Zaidan Dagli
Cancers 2024, 16(4), 820; https://doi.org/10.3390/cancers16040820 - 18 Feb 2024
Cited by 1 | Viewed by 1512
Abstract
Mammary cancer is highly prevalent in non-castrated female dogs. Cell-to-cell communication is an important mechanism to maintain homeostasis, and connexins are proteins that assemble to form the communicating gap junctions. In many cancers, communication capacity is reduced; several approaches are being tested in [...] Read more.
Mammary cancer is highly prevalent in non-castrated female dogs. Cell-to-cell communication is an important mechanism to maintain homeostasis, and connexins are proteins that assemble to form the communicating gap junctions. In many cancers, communication capacity is reduced; several approaches are being tested in order to increase the communication capacity in cancer cells and, therefore, alter their viability. This study analyzed the effects of the alpha-connexin carboxyl-terminal peptide (αCT1) on canine mammary non-neoplastic and neoplastic epithelial cells. Seven canine epithelial mammary cell lines were used. Among these, one was a normal canine epithelial mammary cell line (LOEC-NMG), two canine mammary adenomas (LOEC-MAd1 and LOEC-MAd2), and four canine mammary adenocarcinomas (LOEC-MCA1, LOEC-MCA2, LOEC-MCA3 and CF41). The αCT1 corresponds to a short Cx43 C-terminal sequence linked to an internalization sequence called the antennapedia. After 24 h of incubation, the medium containing different αCT1 peptide concentrations was added to the cells, and only the culture medium was used for control. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test was used to quantify cell viability before treatment and 48, 72, and 96 h after the treatment. Results showed that the normal mammary epithelial cell line (LOEC-NMG) was resistant to treatment with αCT1, which is consistent with a previous study on human mammary cell lines. One of the adenoma cell lines (LOEC-MAd2) was also resistant to treatment with αCT1, although the other (LOEC-MAd1) was susceptible to treatment, mostly at 72 h after treatment. Regarding the four canine adenocarcinoma cell lines, they differ regarding the susceptibility to the treatment with αCT1. Three cell lines, canine mixed adenocarcinoma (LOEC-MCA1), canine complex adenocarcinoma (LOEC-MCA2), and commercial canine mammary adenocarcinoma cell line CF41, were susceptible to treatment with αCT1, while one canine mammary adenocarcinoma cell line (LOEC-MCA3) was resistant to treatment. In most αCT1 treated cell lines, Cx43 was strongly detected in cell membranes by immunofluorescence. We propose that αCT1 restored the cell-to-cell communication capacity of neoplastic cells and induced inhibitory effects on cell viability. Full article
(This article belongs to the Special Issue Cellular Communication, Carcinogenesis and Targeted Interventions)
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14 pages, 3947 KiB  
Article
Mapping the Anti-Cancer Activity of α-Connexin Carboxyl-Terminal (aCT1) Peptide in Resistant HER2+ Breast Cancer
by Kimberly M. Baker, Melissa Abt, Emma H. Doud, Adrian L. Oblak and Elizabeth S. Yeh
Cancers 2024, 16(2), 423; https://doi.org/10.3390/cancers16020423 - 19 Jan 2024
Cited by 1 | Viewed by 1956
Abstract
Connexin 43 (Cx43) is a protein encoded by the GJA1 gene and is a component of cell membrane structures called gap junctions, which facilitate intercellular communication. Prior evidence indicates that elevated GJA1 expression in the HER2-positive (HER2+) subtype of breast cancer is associated [...] Read more.
Connexin 43 (Cx43) is a protein encoded by the GJA1 gene and is a component of cell membrane structures called gap junctions, which facilitate intercellular communication. Prior evidence indicates that elevated GJA1 expression in the HER2-positive (HER2+) subtype of breast cancer is associated with poor prognosis. Prior evidence also suggests that HER2+ breast cancers that have become refractory to HER2-targeted agents have a loss of Cx43 gap junction intercellular communication (GJIC). In this study, a Cx43-targeted agent called alpha-connexin carboxyl-terminal peptide (aCT1) is examined to determine whether GJIC can be rescued in refractory HER2+ breast cancer cells. A proposed mechanism of action for aCT1 is binding to the tight junction protein Zonal Occludens-1 (ZO-1). However, the true scope of activity for aCT1 has not been explored. In this study, mass spectrometry proteomic analysis is used to determine the breadth of aCT1-interacting proteins. The NanoString nCounter Breast Cancer 360 panel is also used to examine the effect of aCT1 on cancer signaling in HER2+ breast cancer cells. Findings from this study show a dynamic range of binding partners for aCT1, many of which regulate gene expression and RNA biology. nCounter analysis shows that a number of pathways are significantly impacted by aCT1, including upregulation of apoptotic factors, leading to the prediction and demonstration that aCT1 can boost the cell death effects of cisplatin and lapatinib in HER2+ breast cancer cells that have become resistant to HER2-targeted agents. Full article
(This article belongs to the Special Issue Cellular Communication, Carcinogenesis and Targeted Interventions)
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