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Breast Cancer, Metastatic Breast Cancer, Therapeutic Approaches 2.0

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

Deadline for manuscript submissions: 21 June 2024 | Viewed by 6133

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Special Issue Editor

Dr. Mi Kyung Park

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Guest Editor

Department of BioHealthcare, Hwasung Medi-Science University, Hwaseong-si 18274, Gyeonggi-do, Republic of Korea
Interests: molecular mechanism; tumor microenvironment; epithelial-to-mesenchymal transition (EMT); post-translational modification (PTM); autophagy; potential therapeutic approaches; preclinical mouse models for cancers; breast cancer; liver cancer; lung cancer; pancreatic cancer; cancer progression and metastasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Breast cancers are heterogeneous and have a multistep progression at molecular and morphologic levels during tumor development. Metastatic breast cancer is a cancer that originated from the breast and that has dispersed into the lymph nodes or to several other sites, such as the bone, liver, lung, or brain, and has acquired genetic and epigenetic alterations in cancer cells. The molecular mechanisms of the epithelial-to-mesenchymal transition (EMT) are provided as therapeutic targets in metastatic breast cancer. Metastasis is a multistage process that is involved in various epigenetic and post-translational modifications (PTMs) during breast cancer progression and metastasis. The remodeling between the tumor microenvironment and the extracellular matrix (ECM) is also essential for metastasis. Various elements of the breast tumor microenvironment enhance metastatic progression.

This Special Issue, “Breast Cancer, Metastatic Breast Cancer, Therapeutic Approaches 2.0”, aims to provide a platform for obtaining new deeper insights into the molecular mechanisms and potential therapeutic approaches in cancer. Authors are invited to submit original research and topical review articles on these topics.

Dr. Mi Kyung Park
Guest Editor

Manuscript Submission Information

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Keywords

breast cancer
metastatic breast cancer
epithelial-to-mesenchymal transition (EMT)
epigenetic and post-translational modifications (PTM)
tumor microenvironment

Published Papers (5 papers)

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Research

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19 pages, 4457 KiB

Open AccessArticle

Modulated Electro-Hyperthermia Accelerates Tumor Delivery and Improves Anticancer Activity of Doxorubicin Encapsulated in Lyso-Thermosensitive Liposomes in 4T1-Tumor-Bearing Mice

by Kenan Aloss, Syeda Mahak Zahra Bokhari, Pedro Henrique Leroy Viana, Nino Giunashvili, Csaba András Schvarcz, Gábor Szénási, Dániel Bócsi, Zoltán Koós, Gert Storm, Zsuzsanna Miklós, Zoltán Benyó and Péter Hamar

Int. J. Mol. Sci. 2024, 25(6), 3101; https://doi.org/10.3390/ijms25063101 - 7 Mar 2024

Viewed by 790

Abstract

Modulated electro-hyperthermia (mEHT) is an adjuvant cancer therapy that enables tumor-selective heating (+2.5 °C). In this study, we investigated whether mEHT accelerates the tumor-specific delivery of doxorubicin (DOX) from lyso-thermosensitive liposomal doxorubicin (LTLD) and improves its anticancer efficacy in mice bearing a triple-negative breast cancer cell line (4T1). The 4T1 cells were orthotopically injected into Balb/C mice, and mEHT was performed on days 9, 12, and 15 after the implantation. DOX, LTLD, or PEGylated liposomal DOX (PLD) were administered for comparison. The tumor size and DOX accumulation in the tumor were measured. The cleaved caspase-3 (cC3) and cell proliferation were evaluated by cC3 or Ki67 immunohistochemistry and Western blot. The LTLD+mEHT combination was more effective at inhibiting tumor growth than the free DOX and PLD, demonstrated by reductions in both the tumor volume and tumor weight. LTLD+mEHT resulted in the highest DOX accumulation in the tumor one hour after treatment. Tumor cell damage was associated with cC3 in the damaged area, and with a reduction in Ki67 in the living area. These changes were significantly the strongest in the LTLD+mEHT-treated tumors. The body weight loss was similar in all mice treated with any DOX formulation, suggesting no difference in toxicity. In conclusion, LTLD combined with mEHT represents a novel approach for DOX delivery into cancer tissue. Full article

(This article belongs to the Special Issue Breast Cancer, Metastatic Breast Cancer, Therapeutic Approaches 2.0)

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Graphical abstract

15 pages, 11448 KiB

Open AccessArticle

Loss of MXRA8 Delays Mammary Tumor Development and Impairs Metastasis

by Kaitlyn E. Simpson, Christina A. Staikos, Katrina L. Watson and Roger A. Moorehead

Int. J. Mol. Sci. 2023, 24(18), 13730; https://doi.org/10.3390/ijms241813730 - 6 Sep 2023

Viewed by 1178

Abstract

Matrix-remodeling-associated protein 8 or MXRA8 is a transmembrane protein that can bind arthritogenic alpha viruses like the Chikungunya virus and provide viral entry into cells. MXRA8 can also interact with integrin β3 and thus possibly regulate cell–cell interactions and binding to the extracellular matrix. While MXRA8 has been associated with reduced survival in patients with colorectal and renal clear cell cancers, the role of MXRA8 in breast cancer remains largely unexplored. Therefore, the aim of this research was to determine the role of MXRA8 in breast cancer by knocking out MXRA8 in the human triple-negative breast cancer cell line MDA-MB-231. The loss of MXRA8 reduced cell proliferation in vitro but had no effect on apoptosis or migration in cultured cells. However, the loss of MXRA8 significantly delayed tumor development and reduced metastatic dissemination to the lungs in a xenograft model. RNA sequencing identified three genes, ADMATS1, TIE1, and BMP2, whose expression were significantly reduced in MXRA8-knockout tumors compared to control tumors. MXRA8 staining of a human breast cancer tissue array revealed higher levels of MXRA8 in primary tumors and metastases of aggressive tumor subtypes (TNBC and HER2⁺) compared to less aggressive, ER⁺ breast cancers. Our findings demonstrate for the first time that MXRA8 regulates the progression of human TNBC possibly through influencing the interaction of tumor cells with their microenvironment. Full article

(This article belongs to the Special Issue Breast Cancer, Metastatic Breast Cancer, Therapeutic Approaches 2.0)

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Review

Jump to: Research

30 pages, 2548 KiB

Open AccessReview

Unraveling the Role of Ras Homolog Enriched in Brain (Rheb1 and Rheb2): Bridging Neuronal Dynamics and Cancer Pathogenesis through Mechanistic Target of Rapamycin Signaling

by Mostafizur Rahman, Tuan Minh Nguyen, Gi Jeong Lee, Boram Kim, Mi Kyung Park and Chang Hoon Lee

Int. J. Mol. Sci. 2024, 25(3), 1489; https://doi.org/10.3390/ijms25031489 - 25 Jan 2024

Viewed by 954

Abstract

Ras homolog enriched in brain (Rheb1 and Rheb2), small GTPases, play a crucial role in regulating neuronal activity and have gained attention for their implications in cancer development, particularly in breast cancer. This study delves into the intricate connection between the multifaceted functions of Rheb1 in neurons and cancer, with a specific focus on the mTOR pathway. It aims to elucidate Rheb1’s involvement in pivotal cellular processes such as proliferation, apoptosis resistance, migration, invasion, metastasis, and inflammatory responses while acknowledging that Rheb2 has not been extensively studied. Despite the recognized associations, a comprehensive understanding of the intricate interplay between Rheb1 and Rheb2 and their roles in both nerve and cancer remains elusive. This review consolidates current knowledge regarding the impact of Rheb1 on cancer hallmarks and explores the potential of Rheb1 as a therapeutic target in cancer treatment. It emphasizes the necessity for a deeper comprehension of the molecular mechanisms underlying Rheb1-mediated oncogenic processes, underscoring the existing gaps in our understanding. Additionally, the review highlights the exploration of Rheb1 inhibitors as a promising avenue for cancer therapy. By shedding light on the complicated roles between Rheb1/Rheb2 and cancer, this study provides valuable insights to the scientific community. These insights are instrumental in guiding the identification of novel targets and advancing the development of effective therapeutic strategies for treating cancer. Full article

(This article belongs to the Special Issue Breast Cancer, Metastatic Breast Cancer, Therapeutic Approaches 2.0)

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23 pages, 2323 KiB

Open AccessReview

CDKN1A/p21 in Breast Cancer: Part of the Problem, or Part of the Solution?

by Evangelos Manousakis, Clàudia Martinez Miralles, Maria Guimerà Esquerda and Roni H. G. Wright

Int. J. Mol. Sci. 2023, 24(24), 17488; https://doi.org/10.3390/ijms242417488 - 14 Dec 2023

Cited by 2 | Viewed by 1491

Abstract

Cyclin-dependent kinase inhibitor 1A (Cip1/Waf1/CDKN1A/p21) is a well-established protein, primarily recognised for its pivotal role in the cell cycle, where it induces cell cycle arrest by inhibiting the activity of cyclin-dependent kinases (CDKs). Over the years, extensive research has shed light on various additional mechanisms involving CDKN1A/p21, implicating it in processes such as apoptosis, DNA damage response (DDR), and the regulation of stem cell fate. Interestingly, p21 can function either as an oncogene or as a tumour suppressor in these contexts. Complicating matters further, the expression of CDKN1A/p21 is elevated in certain tumour types while downregulated in others. In this comprehensive review, we provide an overview of the multifaceted functions of CDKN1A/p21, present clinical data pertaining to cancer patients, and delve into potential strategies for targeting CDKN1A/p21 as a therapeutic approach to cancer. Manipulating CDKN1A/p21 shows great promise for therapy given its involvement in multiple cancer hallmarks, such as sustained cell proliferation, the renewal of cancer stem cells (CSCs), epithelial–mesenchymal transition (EMT), cell migration, and resistance to chemotherapy. Given the dual role of CDKN1A/p21 in these processes, a more in-depth understanding of its specific mechanisms of action and its regulatory network is imperative to establishing successful therapeutic interventions. Full article

(This article belongs to the Special Issue Breast Cancer, Metastatic Breast Cancer, Therapeutic Approaches 2.0)

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14 pages, 1133 KiB

Open AccessReview

Semaphorins and Their Roles in Breast Cancer: Implications for Therapy Resistance

by Radhika Aiyappa-Maudsley, Louis F. V. McLoughlin and Thomas A. Hughes

Int. J. Mol. Sci. 2023, 24(17), 13093; https://doi.org/10.3390/ijms241713093 - 23 Aug 2023

Viewed by 1268

Abstract

Breast cancer is the most common cancer worldwide and a leading cause of cancer-related deaths in women. The clinical management of breast cancer is further complicated by the heterogeneous nature of the disease, which results in varying prognoses and treatment responses in patients. The semaphorins are a family of proteins with varied roles in development and homoeostasis. They are also expressed in a wide range of human cancers and are implicated as regulators of tumour growth, angiogenesis, metastasis and immune evasion. More recently, semaphorins have been implicated in drug resistance across a range of malignancies. In breast cancer, semaphorins are associated with resistance to endocrine therapy as well as breast cancer chemotherapeutic agents such as taxanes and anthracyclines. This review will focus on the semaphorins involved in breast cancer progression and their association with drug resistance. Full article

(This article belongs to the Special Issue Breast Cancer, Metastatic Breast Cancer, Therapeutic Approaches 2.0)

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