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Breast Cancer: From Molecular and Cellular Mechanisms to Novel Therapeutic Approaches

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A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (1 June 2021) | Viewed by 13083

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Special Issue Editors

Prof. Malathy Shekhar

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Guest Editor

Department of Oncology, Wayne State University School of Medicine, Detroit, MI, USA
Interests: breast cancer; DNA damage response and repair; cell signaling mechanisms; drug resistance

Prof. Michael S. Simon

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Guest Editor

Department of Oncology, Barbara Ann Karmanos Cancer Institute at Wayne State University School of Medicine, Detroit, MI, USA
Interests: cancer genetics; breast cancer; racial disparities

Special Issue Information

Dear Colleagues,

The focus of this Special Issue is original articles and thought-provoking reviews and commentaries that investigate or address important questions relevant to breast cancer development, metastasis, treatment, and therapy resistance. This Special Issue will cover topics that are related to the molecular and cellular basis of breast cancer development, progression and metastasis, as well as preclinical and clinical studies with a biological basis. Topics pertinent to breast cancer biology may include breast cancer models, genomics, tumor heterogeneity, tumor microenvironment and interactions, disease markers and therapeutic targets, drug response and resistance mechanisms, metabolism, cancer stem cells, plasticity, circulating tumor cells, cell signaling, and DNA damage response mechanisms. Additionally, translational, preclinical and clinical studies focused on novel therapies, diagnosis, risk stratification, and management of breast cancer with a biological basis are of particular interest.

We look forward to your contributions to this Special Issue.

Prof. Malathy Shekhar
Prof. Michael S. Simon
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. Cells 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 2700 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 signaling mechanisms
DNA damage response and repair
tumor stromal interactions
cell metabolism
drug resistance

Published Papers (3 papers)

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Research

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18 pages, 4104 KiB

Open AccessArticle

Identification of the Novel Tumor Suppressor Role of FOCAD/miR-491-5p to Inhibit Cancer Stemness, Drug Resistance and Metastasis via Regulating RABIF/MMP Signaling in Triple Negative Breast Cancer

by Wei-Chieh Huang, Hsiang-Cheng Chi, Shiao-Lin Tung, Po-Ming Chen, Ya-Chi Shih, Yi-Ching Huang and Pei-Yi Chu

Cells 2021, 10(10), 2524; https://doi.org/10.3390/cells10102524 - 24 Sep 2021

Cited by 7 | Viewed by 2636

Abstract

Triple negative breast cancer (TNBC) possesses poor prognosis mainly due to development of chemoresistance and lack of effective endocrine or targeted therapies. MiR-491-5p has been found to play a tumor suppressor role in many cancers including breast cancer. However, the precise role of miR-491-5p in TNBC has never been elucidated. In this study, we reported the novel tumor suppressor function of FOCAD/miR-491-5p in TNBC. High expression of miR-491-5p was found to be associated with better overall survival in breast cancer patients. We found that miR-491-5p could be an intronic microRNA processed form FOCAD gene. We are the first to demonstrate that both miR-491-5p and FOCAD function as tumor suppressors to inhibit cancer stemness, epithelial-mesenchymal transition, drug resistance, cell migration/invasion, and pulmonary metastasis etc. in TNBC. MiR-491-5p was first reported to directly target Rab interacting factor (RABIF) to downregulate RABIF-mediated TNBC cancer stemness, drug resistance, cell invasion, and pulmonary metastasis via matrix metalloproteinase (MMP) signaling. High expression of RABIF was found to be correlated with poor clinical outcomes of breast cancer and TNBC patients. Our data indicated that miR-491-5p and RABIF are potential prognostic biomarkers and targeting the novel FOCAD/miR-491-5p/RABIF/MMP signaling pathway could serve as a promising strategy in TNBC treatment. Full article

(This article belongs to the Special Issue Breast Cancer: From Molecular and Cellular Mechanisms to Novel Therapeutic Approaches)

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15 pages, 5296 KiB

Open AccessFeature PaperArticle

Extracellular Matrix Components Regulate Bone Sialoprotein Expression in MDA-MB-231 Breast Cancer Cells

by Florian Keller, Roman Bruch, Franziska Clauder, Mathias Hafner and Rüdiger Rudolf

Cells 2021, 10(6), 1304; https://doi.org/10.3390/cells10061304 - 24 May 2021

Cited by 1 | Viewed by 3292

Abstract

Bone sialoprotein (BSP) has become a target in breast cancer research as it is associated with tumor progression and metastasis. The mechanisms underlying the regulation of BSP expression have been largely elusive. Given that BSP is involved in the homing of cancer cells in bone metastatic niches, we addressed regulatory effects of proteolytic cleavage and extracellular matrix components on BSP expression and distribution in cell culture models. Therefore, MDA-MB-231 human breast cancer cells were kept in 2D and 3D spheroid cultures and exposed to basement membrane extract in the presence or absence of matrix metalloproteinase 9 or the non-polar protease, dispase. Confocal imaging of immunofluorescence samples stained with different antibodies against human BSP demonstrated a strong inducing effect of basement membrane extract on anti-BSP immunofluorescence. Similarly, protease incubation led to acute upregulation of anti-BSP immunofluorescence signals, which was blocked by cycloheximide, suggesting de novo formation of BSP. In summary, our data show that extracellular matrix components play an important function in regulating BSP expression and hint at mechanisms for the formation of bone-associated metastasis in breast cancer that might involve local control of BSP levels by extracellular matrix degradation and release of growth factors. Full article

(This article belongs to the Special Issue Breast Cancer: From Molecular and Cellular Mechanisms to Novel Therapeutic Approaches)

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Review

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15 pages, 981 KiB

Open AccessReview

Novel Peptide Therapeutic Approaches for Cancer Treatment

by Caroline M. Li, Pouya Haratipour, Robert G. Lingeman, J. Jefferson P. Perry, Long Gu, Robert J. Hickey and Linda H. Malkas

Cells 2021, 10(11), 2908; https://doi.org/10.3390/cells10112908 - 27 Oct 2021

Cited by 50 | Viewed by 6375

Abstract

Peptides are increasingly being developed for use as therapeutics to treat many ailments, including cancer. Therapeutic peptides have the advantages of target specificity and low toxicity. The anticancer effects of a peptide can be the direct result of the peptide binding its intended target, or the peptide may be conjugated to a chemotherapy drug or radionuclide and used to target the agent to cancer cells. Peptides can be targeted to proteins on the cell surface, where the peptide–protein interaction can initiate internalization of the complex, or the peptide can be designed to directly cross the cell membrane. Peptides can induce cell death by numerous mechanisms including membrane disruption and subsequent necrosis, apoptosis, tumor angiogenesis inhibition, immune regulation, disruption of cell signaling pathways, cell cycle regulation, DNA repair pathways, or cell death pathways. Although using peptides as therapeutics has many advantages, peptides have the disadvantage of being easily degraded by proteases once administered and, depending on the mode of administration, often have difficulty being adsorbed into the blood stream. In this review, we discuss strategies recently developed to overcome these obstacles of peptide delivery and bioavailability. In addition, we present many examples of peptides developed to fight cancer. Full article

(This article belongs to the Special Issue Breast Cancer: From Molecular and Cellular Mechanisms to Novel Therapeutic Approaches)

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