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Molecular Pathways and New Therapies for Breast Cancer

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

Deadline for manuscript submissions: 20 April 2025 | Viewed by 2196

Special Issue Editor


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Guest Editor
Meharry Medical College, Nashville, TN 37208, USA
Interests: molecular; determinants; cancer metastasis; fetuin-A; galectin-3; prostate cancer; breast cancer
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Special Issue Information

Dear Colleagues,

Breast cancer is the most common malignancy in women worldwide. Due to its heterogeneity, the molecular mechanisms governing breast cancer development and progression are complex and impact prognosis and treatment efficacy. Depending on the expression of the estrogen receptor, the progesterone receptor, and the human epidermal growth factor receptor 2 (HER2), breast cancer can be classified as luminal, HER2-enriched, and triple-negative. Each sub-type possesses different treatment strategies, prognostic, and treatment response rates. Therefore, investigating molecular mechanisms of tumor progression, resistance and metastasis is crucial to better understand and identify at-risk patients and develop novel targets and treatment strategies in order to improve breast cancer patient prognosis.

The goals of this Research Topic are to elucidate the molecular mechanisms underlying cancer progression in patients with breast cancer. We aim to focus on identifying novel intrinsic and extrinsic molecular pathways. Furthermore, we will also focus on novel treatment proposals and innovative approaches to develop novel treatments and better identify patients who are at high risk of failing current standard approaches.

This Special Issue of IJMS will welcome original research and review articles discussing novel signaling pathways and therapy in breast cancer.

Dr. Josiah Ochieng
Guest Editor

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Keywords

  • breast cancer
  • cell signaling
  • molecular heterogeneity
  • targeted therapies
  • HER2
  • biomarkers

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Published Papers (2 papers)

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Research

19 pages, 2242 KiB  
Article
A Computational Recognition Analysis of Promising Prognostic Biomarkers in Breast, Colon and Lung Cancer Patients
by Tala Bakheet, Nada Al-Mutairi, Mosaab Doubi, Wijdan Al-Ahmadi, Khaled Alhosaini and Fahad Al-Zoghaibi
Int. J. Mol. Sci. 2025, 26(3), 1017; https://doi.org/10.3390/ijms26031017 - 25 Jan 2025
Viewed by 407
Abstract
Breast, colon, and lung carcinomas are classified as aggressive tumors with poor relapse-free survival (RFS), progression-free survival (PF), and poor hazard ratios (HRs) despite extensive therapy. Therefore, it is essential to identify a gene expression signature that correlates with RFS/PF and HR status [...] Read more.
Breast, colon, and lung carcinomas are classified as aggressive tumors with poor relapse-free survival (RFS), progression-free survival (PF), and poor hazard ratios (HRs) despite extensive therapy. Therefore, it is essential to identify a gene expression signature that correlates with RFS/PF and HR status in order to predict treatment efficiency. RNA-binding proteins (RBPs) play critical roles in RNA metabolism, including RNA transcription, maturation, and post-translational regulation. However, their involvement in cancer is not yet fully understood. In this study, we used computational bioinformatics to classify the functions and correlations of RBPs in solid cancers. We aimed to identify molecular biomarkers that could help predict disease prognosis and improve the therapeutic efficiency in treated patients. Intersection analysis summarized more than 1659 RBPs across three recently updated RNA databases. Bioinformatics analysis showed that 58 RBPs were common in breast, colon, and lung cancers, with HR values < 1 and >1 and a significant Q-value < 0.0001. RBP gene clusters were identified based on RFS/PF, HR, p-value, and fold induction. To define union RBPs, common genes were subjected to hierarchical clustering and were classified into two groups. Poor survival was associated with high genes expression, including CDKN2A, MEX3A, RPL39L, VARS, GSPT1, SNRPE, SSR1, and TIA1 in breast and colon cancer but not with lung cancer; and poor survival was associated with low genes expression, including PPARGC1B, EIF4E3, and SMAD9 in breast, colon, and lung cancer. This study highlights the significant contribution of PPARGC1B, EIF4E3, and SMAD9 out of 11 RBP genes as prognostic predictors in patients with breast, colon, and lung cancers and their potential application in personalized therapy. Full article
(This article belongs to the Special Issue Molecular Pathways and New Therapies for Breast Cancer)
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19 pages, 5244 KiB  
Article
Overexpression of Glyoxalase 2 in Human Breast Cancer Cells: Implications for Cell Proliferation and Doxorubicin Resistance
by Brenda Romaldi, Andrea Scirè, Cristina Minnelli, Andrea Frontini, Giulia Casari, Laura Cianfruglia, Giovanna Mobbili, Lidia de Bari, Cinzia Antognelli, Federico V. Pallardó and Tatiana Armeni
Int. J. Mol. Sci. 2024, 25(20), 10888; https://doi.org/10.3390/ijms252010888 - 10 Oct 2024
Viewed by 1005
Abstract
Glyoxalase 2 (Glo2) is an enzyme of the glyoxalase system whose pathway parallels glycolysis and which aims to remove methylglyoxal (MGO). This study analyzed the possible additional roles of the Glo2 enzyme in breast cancer (MCF7) and non-cancer (HDF) cell lines, investigating its [...] Read more.
Glyoxalase 2 (Glo2) is an enzyme of the glyoxalase system whose pathway parallels glycolysis and which aims to remove methylglyoxal (MGO). This study analyzed the possible additional roles of the Glo2 enzyme in breast cancer (MCF7) and non-cancer (HDF) cell lines, investigating its presence at the nuclear level and its potential involvement in cell proliferation and chemotherapy resistance. The results revealed that Glo2 is overexpressed in cancer cells, and its expression is higher during the proliferative (S and G2/M) phases of the cell cycle. The study also examined a post-translational modification (PTM) in which Glo2 could be involved, with S-glutathionylation revealing that Glo2 enhances this PTM in cancer cells both in the cytoplasm and nucleus. Inhibition of Glo2 by p-NCBG resulted in increased sensitivity to doxorubicin, a common chemotherapeutic agent. This suggests that Glo2 increases cancer cell resistance to chemotherapy, potentially through its role in regulating oxidative stress. These results highlight Glo2 as a potential therapeutic target to improve the efficacy of existing treatments. Full article
(This article belongs to the Special Issue Molecular Pathways and New Therapies for Breast Cancer)
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