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Molecular Research in Breast Cancer: Pathophysiology and Treatment
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Molecular Research in Breast Cancer: Pathophysiology and Treatment

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 (30 April 2024) | Viewed by 1989

Special Issue Editor

Dr. Costa Frangou

E-Mail Website
Guest Editor
Department of Molecular and Cellular Biology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA
Interests: breast cancer

Special Issue Information

Dear Colleagues,

Breast cancer is a complex, heterogeneous disease that can be divided into distinct clinical, histopathological, and molecular subtypes. Breast cancer survival rates have improved significantly in recent decades due to early detection, better screening, and improvements in treatment options; however, 20%–30% of breast cancers progress to recurrent or metastatic disease. Recently, it has been shown that breast cancer consists not only of neoplastic cells but also of alterations in the tumor microenvironment. These alterations are now recognized as critical in breast cancer development and progression. Questions remain as to why many types of breast cancer do not respond well to targeted treatments, particularly immunotherapy. Furthermore, targeted therapy for breast cancer also faces the challenges of increasing cancer care costs and the risk of overtreatment. Future progress in breast cancer treatment and diagnosis will require new molecular targets and diagnostic biomarkers in order to improve patient prognoses and therapy outcomes.

Dr. Costa Frangou
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 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

  • breast
  • biomarker
  • early detection
  • immunotherapy
  • metastasis
  • microenvironment
  • outcomes
  • prognosis
  • relapse
  • treatment
  • tumor

Published Papers (2 papers)

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Research

15 pages, 2965 KiB  
Article
Soluble NKG2DLs Are Elevated in Breast Cancer Patients and Associate with Disease Outcome
by Anna Seller, Christian M. Tegeler, Jonas Mauermann, Tatjana Schreiber, Ilona Hagelstein, Kai Liebel, André Koch, Jonas S. Heitmann, Sarah M. Greiner, Clara Hayn, Dominik Dannehl, Tobias Engler, Andreas D. Hartkopf, Markus Hahn, Sara Y. Brucker, Helmut R. Salih and Melanie Märklin
Int. J. Mol. Sci. 2024, 25(7), 4126; https://doi.org/10.3390/ijms25074126 - 08 Apr 2024
Viewed by 672
Abstract
Ligands of the natural killer group 2D (NKG2DL) family are expressed on malignant cells and are usually absent from healthy tissues. Recognition of NKG2DLs such as MICA/B and ULBP1-3 by the activating immunoreceptor NKG2D, expressed by NK and cytotoxic T cells, stimulates anti-tumor [...] Read more.
Ligands of the natural killer group 2D (NKG2DL) family are expressed on malignant cells and are usually absent from healthy tissues. Recognition of NKG2DLs such as MICA/B and ULBP1-3 by the activating immunoreceptor NKG2D, expressed by NK and cytotoxic T cells, stimulates anti-tumor immunity in breast cancer. Upregulation of membrane-bound NKG2DLs in breast cancer has been demonstrated by immunohistochemistry. Tumor cells release NKG2DLs via proteolytic cleavage as soluble (s)NKG2DLs, which allows for effective immune escape and is associated with poor prognosis. In this study, we collected serum from 140 breast cancer (BC) and 20 ductal carcinoma in situ (DCIS) patients at the time of initial diagnosis and 20 healthy volunteers (HVs). Serum levels of sNKG2DLs were quantified through the use of ELISA and correlated with clinical data. The analyzed sNKG2DLs were low to absent in HVs and significantly higher in BC patients. For some of the ligands analyzed, higher sNKG2DLs serum levels were associated with the classification of malignant tumor (TNM) stage and grading. Low sMICA serum levels were associated with significantly longer progression-free (PFS) and overall survival (OS). In conclusion, we provide the first insights into sNKG2DLs in BC patients and suggest their potential role in tumor immune escape in breast cancer. Furthermore, our observations suggest that serum sMICA levels may serve as a prognostic parameter in the patients analyzed in this study. Full article
(This article belongs to the Special Issue Molecular Research in Breast Cancer: Pathophysiology and Treatment)
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18 pages, 3354 KiB  
Article
miRNA-378 Is Downregulated by XBP1 and Inhibits Growth and Migration of Luminal Breast Cancer Cells
by Vahid Arabkari, David Barua, Muhammad Mosaraf Hossain, Mark Webber, Terry Smith, Ananya Gupta and Sanjeev Gupta
Int. J. Mol. Sci. 2024, 25(1), 186; https://doi.org/10.3390/ijms25010186 - 22 Dec 2023
Cited by 1 | Viewed by 902
Abstract
X-box binding protein 1 (XBP1) is a transcription factor that plays a crucial role in the unfolded protein response (UPR), a cellular stress response pathway involved in maintaining protein homeostasis in the endoplasmic reticulum (EnR). While the role of XBP1 in UPR is [...] Read more.
X-box binding protein 1 (XBP1) is a transcription factor that plays a crucial role in the unfolded protein response (UPR), a cellular stress response pathway involved in maintaining protein homeostasis in the endoplasmic reticulum (EnR). While the role of XBP1 in UPR is well-characterised, emerging evidence suggests its involvement in endocrine resistance in breast cancer. The transcriptional activity of spliced XBP1 (XBP1s) is a major component of its biological effects, but the targets of XBP1s in estrogen receptor (ER)-positive breast cancer are not well understood. Here, we show that the expression of miR-378 and PPARGC1B (host gene of miR-378) is downregulated during UPR. Using chemical and genetic methods, we show that XBP1s is necessary and sufficient for the downregulation of miR-378 and PPARGC1B. Our results show that overexpression of miR-378 significantly suppressed cell growth, colony formation, and migration of ER-positive breast cancer cells. Further, we found that expression of miR-378 sensitised the cells to UPR-induced cell death and anti-estrogens. The expression of miR-378 and PPARGC1B was downregulated in breast cancer, and higher expression of miR-378 is associated with better outcomes in ER-positive breast cancer. We found that miR-378 upregulates the expression of several genes that regulate type I interferon signalling. Analysis of separate cohorts of breast cancer patients showed that a gene signature derived from miR-378 upregulated genes showed a strong association with improved overall and recurrence-free survival in breast cancer. Our results suggest a growth-suppressive role for miR-378 in ER-positive breast cancer where downregulation of miR-378 by XBP1 contributes to endocrine resistance in ER-positive breast cancer. Full article
(This article belongs to the Special Issue Molecular Research in Breast Cancer: Pathophysiology and Treatment)
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