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Life
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Drug Resistance, Molecular Oncology and Genetics of Breast Cancer
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Drug Resistance, Molecular Oncology and Genetics of Breast Cancer

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (17 December 2021) | Viewed by 4768

Special Issue Editors

Dr. Ui-Soon Khoo

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Guest Editor
Department of Pathology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China
Interests: drug resistance; breast cancer; molecular oncology
Dr. Ho Tsoi

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Guest Editor
Department of Pathology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China
Interests: cancer biology; drug resistance; biomarkers
Dr. Man-Hong Leung

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Guest Editor
Department of Pathology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China
Interests: cancer biology; drug resistance; biomarkers

Special Issue Information

Dear Colleagues,

There has been rapid growth in our knowledge of breast cancer biology and molecular genetics, which has led to a better understanding of this heterogeneous disease, both in terms of its progression as well as improved treatment modalities. Advances in our understanding have facilitated the development of targeted therapy as well as new therapeutic strategies that have greatly improved disease outcome as well as survival.

Understanding, dissecting and connecting novel breast cancer mechanistic networks requires multidisciplinary approaches. This Special Issue, “Drug Resistance, Molecular Oncology and Genetics of Breast Cancer”, provides the opportunity for scientists and clinicians to present research articles as well as reviews on cutting-edge discoveries in the field of mechanisms underlying breast cancer pathogenesis and therapeutic strategies aimed at targeting deregulated signaling pathways in breast cancer.

Dr. Ui-Soon Khoo
Dr. Ho Tsoi
Dr. Man-Hong Leung
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. Life is an international peer-reviewed open access monthly 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 2600 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

  • breast cancer
  • triple-negative breast cancer
  • her2-positive breast cancer
  • estrogen receptor positive breast cancer
  • targeted therapy
  • molecular pathogenesis
  • mechanisms of drug resistance
  • genetic profiling
  • novel approaches to treatment

Published Papers (2 papers)

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Research

21 pages, 4484 KiB  
Article
Overexpression of BQ323636.1 Modulated AR/IL-8/CXCR1 Axis to Confer Tamoxifen Resistance in ER-Positive Breast Cancer
by Ho Tsoi, Ling Shi, Man-Hong Leung, Ellen P. S. Man, Zi-Qing So, Wing-Lok Chan and Ui-Soon Khoo
Life 2022, 12(1), 93; https://doi.org/10.3390/life12010093 - 10 Jan 2022
Cited by 4 | Viewed by 1669
Abstract
NCOR2 is a co-repressor for estrogen receptor (ER) and androgen receptor (AR). Our group previously identified a novel splice variant of NCOR2, BQ323636.1 (BQ), that mediates tamoxifen resistance via interference of NCOR2 repression on ER. Luciferase reporter assay showed BQ overexpression could enhance [...] Read more.
NCOR2 is a co-repressor for estrogen receptor (ER) and androgen receptor (AR). Our group previously identified a novel splice variant of NCOR2, BQ323636.1 (BQ), that mediates tamoxifen resistance via interference of NCOR2 repression on ER. Luciferase reporter assay showed BQ overexpression could enhance the transcriptional activity of androgen response element (ARE). We proposed that BQ employs both AR and ER to confer tamoxifen resistance. Through in silico analysis, we identified interleukin-8 (IL-8) as the sole ERE and ARE containing gene responsiveness to ER and AR activation. We confirmed that BQ overexpression enhanced the expression of IL-8 in ER+ve breast cancer cells, and AR inhibition reduced IL-8 expression in the BQ overexpressing cell lines, suggesting that AR was involved in the modulation of IL-8 expression by BQ. Moreover, we demonstrated that IL-8 could activate both AKT and ERK1/2 via CXCR1 to confer tamoxifen resistance. Targeting CXCR1/2 by a small inhibitor repertaxin reversed tamoxifen resistance of BQ overexpressing breast cancer cells in vitro and in vivo. In conclusion, BQ overexpression in ER+ve breast cancer can enhance IL-8 mediated signaling to modulate tamoxifen resistance. Targeting IL-8 signaling is a promising approach to overcome tamoxifen resistance in ER+ve breast cancer. Full article
(This article belongs to the Special Issue Drug Resistance, Molecular Oncology and Genetics of Breast Cancer)
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13 pages, 15306 KiB  
Article
Role of PTEN, PI3K, and mTOR in Triple-Negative Breast Cancer
by Mirjana Prvanović, Milica Nedeljković, Nasta Tanić, Tijana Tomić, Tanja Terzić, Zorka Milovanović, Zlatko Maksimović and Nikola Tanić
Life 2021, 11(11), 1247; https://doi.org/10.3390/life11111247 - 17 Nov 2021
Cited by 17 | Viewed by 2489
Abstract
Breast cancer is the most commonly occurring malignancy and the leading cause of cancer-related death in women. Triple-negative breast cancer (TNBC) is the most aggressive subtype and is associated with high recurrence rates, high incidence of distant metastases, and poor overall survival. The [...] Read more.
Breast cancer is the most commonly occurring malignancy and the leading cause of cancer-related death in women. Triple-negative breast cancer (TNBC) is the most aggressive subtype and is associated with high recurrence rates, high incidence of distant metastases, and poor overall survival. The aim of this study was to investigate the PI3K/PTEN/Akt/mTOR pathway as one of the most frequently deregulated pathways in cancer. We aimed to explore the impact of PI3K and mTOR oncogenes as well as the PTEN tumor suppressor on TNBC clinical behavior, prognosis, and multidrug resistance (MDR), using immunohistochemistry and copy number analysis by quantitative real-time PCR. Our results revealed that loss of PTEN and high expression of PI3K and mTOR proteins are associated with poor outcome of TNBC patients. PTEN deletions appeared as a major cause of reduced or absent PTEN expression in TNBC. Importantly, homozygous deletions of PTEN (and not hemizygous deletions) are a potential molecular marker of metastasis formation and good predictors of TNBC outcome. In conclusion, we believe that concurrent examination of PTEN/PI3K/mTOR protein expression may be more useful in predicting TNBC clinical course than the analysis of single protein expression. Specifically, our results showed that PTEN-reduced/PI3K-high/mTOR-high expression constitutes a ‘high risk’ profile of TNBC. Full article
(This article belongs to the Special Issue Drug Resistance, Molecular Oncology and Genetics of Breast Cancer)
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