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Cancers
Special Issues
Genetic and Epigenetic Regulation of Cancer Metastasis
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Genetic and Epigenetic Regulation of Cancer Metastasis

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Metastasis".

Deadline for manuscript submissions: closed (15 March 2024) | Viewed by 2298

Special Issue Editors

Dr. Ray-chang Wu

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Medicine, George Washington University, Washington, DC 20037, USA
Interests: nuclear hormone receptors; co-regulators; chromatin remodeling; epigenetics; therapy resistance; anti-tumor immunity
Dr. Mei-Yi Wu

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
Interests: breast cancer; prostate cancer; chromatin remodeling; epigenetics; cancer metastasis

Special Issue Information

Dear Colleagues,

Cancer metastasis accounts for the majority of cancer-related deaths in patients. Metastasis is a complex multi-step process which includes cancer migration, dissemination, extravasation, angiogenesis, and proliferation at the secondary sites. For cancer cells to successfully progress through these different biological steps and survive at distant sites, gene regulation is required in the cancer cells as well as in the host cells that constitute the tumor microenvironment. Understanding the molecular mechanisms and the genetic programs responsible for driving cancer metastasis has been and will continue to be the focus of extensive investigation for years to come. It is expected that insights into the molecular mechanisms, including genetic and epigenetic regulation that control metastasis, will reveal not only new diagnostic and prognostic markers but will also lead to the development of new therapeutics. In this Special Issue of Cancers, we welcome the submission of original research articles that focus on unraveling the cause of cancer metastasis and review articles that discuss our current understanding of the genetic and epigenetic determinants underpinning cancer metastasis.  

Dr. Ray-chang Wu
Dr. Mei-Yi Wu
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. Cancers 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 2900 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

  • tumorigenesis
  • metastasis
  • tumor microenvironment
  • genetic regulation
  • epigenetic regulation
  • epithelial–mesenchymal transition

Published Papers (3 papers)

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Research

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19 pages, 2056 KiB  
Article
TWIST1 Drives Cytotoxic CD8+ T-Cell Exhaustion through Transcriptional Activation of CD274 (PD-L1) Expression in Breast Cancer Cells
by Xiaobin Yu and Jianming Xu
Cancers 2024, 16(11), 1973; https://doi.org/10.3390/cancers16111973 - 22 May 2024
Viewed by 462
Abstract
In breast cancer, epithelial-mesenchymal transition (EMT) is positively associated with programmed death ligand 1 (PD-L1) expression and immune escape, and TWIST1 silences ERα expression and induces EMT and cancer metastasis. However, how TWIST1 regulates PD-L1 and immune evasion is unknown. This study analyzed [...] Read more.
In breast cancer, epithelial-mesenchymal transition (EMT) is positively associated with programmed death ligand 1 (PD-L1) expression and immune escape, and TWIST1 silences ERα expression and induces EMT and cancer metastasis. However, how TWIST1 regulates PD-L1 and immune evasion is unknown. This study analyzed TWIST1 and PD-L1 expression in breast cancers, investigated the mechanism for TWIST1 to regulate PD-L1 transcription, and assessed the effects of TWIST1 and PD-L1 in cancer cells on cytotoxic CD8+ T cells. Interestingly, TWIST1 expression is correlated with high-level PD-L1 expression in ERα-negative breast cancer cells. The overexpression and knockdown of TWIST1 robustly upregulate and downregulate PD-L1 expression, respectively. TWIST1 binds to the PD-L1 promoter and recruits the TIP60 acetyltransferase complex in a BRD8-dependent manner to transcriptionally activate PD-L1 expression, which significantly accelerates the exhaustion and death of the cytotoxic CD8+ T cells. Accordingly, knockdown of TWIST1 or BRD8 or inhibition of PD-L1 significantly enhances the tumor antigen-specific CD8+ T cells to suppress the growth of breast cancer cells. These results demonstrate that TWIST1 directly induces PD-L1 expression in ERα-negative breast cancer cells to promote immune evasion. Targeting TWIST1, BRD8, and/or PD-L1 in ERα-negative breast cancer cells with TWIST1 expression may sensitize CD8+ T-cell-mediated immunotherapy. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Cancer Metastasis)
20 pages, 11490 KiB  
Article
Combination of miR-99b-5p and Enzalutamide or Abiraterone Synergizes the Suppression of EMT-Mediated Metastasis in Prostate Cancer
by Mohammad Waseem and Bi-Dar Wang
Cancers 2024, 16(10), 1933; https://doi.org/10.3390/cancers16101933 - 19 May 2024
Viewed by 499
Abstract
Prostate cancer (PCa) is the most frequently diagnosed cancer and second leading cause of cancer deaths among American men. Androgen deprivation therapy (ADT) has been systemically applied as a first-line therapy for PCa patients. Despite the initial responses, the majority of patients under [...] Read more.
Prostate cancer (PCa) is the most frequently diagnosed cancer and second leading cause of cancer deaths among American men. Androgen deprivation therapy (ADT) has been systemically applied as a first-line therapy for PCa patients. Despite the initial responses, the majority of patients under ADT eventually experienced tumor progression to castration-resistant prostate cancer (CRPC), further leading to tumor metastasis to distant organs. Therefore, identifying the key molecular mechanisms underlying PCa progression remains crucial for the development of novel therapies for metastatic PCa. Previously, we identified that tumor-suppressive miR-99b-5p is frequently downregulated in aggressive African American (AA) PCa and European American (EA) CRPC, leading to upregulation of mTOR, androgen receptor (AR), and HIF-1α signaling. Given the fact that mTOR and HIF-1α signaling are critical upstream pathways that trigger the activation of epithelial–mesenchymal transition (EMT), we hypothesized that miR-99b-5p may play a critical functional role in regulating EMT-mediated PCa metastasis. To test this hypothesis, a series of cell biology, biochemical, and in vitro functional assays (wound healing, transwell migration, cell/ECM adhesion, and capillary-like tube formation assays) were performed to examine the effects of miR-99b-5p mimic on regulating EMT-mediated PCa metastasis processes. Our results have demonstrated that miR-99b-5p simultaneously targets MTOR and AR signaling, leading to upregulation of E-cadherin, downregulation of Snail/N-cadherin/Vimentin, and suppression of EMT-mediated PCa metastasis. MiR-99b-5p alone and in combination with enzalutamide or abiraterone significantly inhibits the EMT-mediated metastasis of AA PCa and EA CRPC. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Cancer Metastasis)
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Review

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16 pages, 1638 KiB  
Review
Role of the Atypical MAPK ERK3 in Cancer Growth and Progression
by Lobna Elkhadragy, Amanda Myers and Weiwen Long
Cancers 2024, 16(7), 1381; https://doi.org/10.3390/cancers16071381 - 31 Mar 2024
Viewed by 773
Abstract
Extracellular signal-regulated kinase 3 (ERK3) is an atypical mitogen-activated protein kinase (MAPK) whose structural and regulatory features are distinct from those of conventional MAPKs, such as ERK1/2. Since its identification in 1991, the regulation, substrates and functions of ERK3 have remained largely unknown. [...] Read more.
Extracellular signal-regulated kinase 3 (ERK3) is an atypical mitogen-activated protein kinase (MAPK) whose structural and regulatory features are distinct from those of conventional MAPKs, such as ERK1/2. Since its identification in 1991, the regulation, substrates and functions of ERK3 have remained largely unknown. However, recent years have witnessed a wealth of new findings about ERK3 signaling. Several important biological functions for ERK3 have been revealed, including its role in neuronal morphogenesis, inflammation, metabolism, endothelial cell tube formation and epithelial architecture. In addition, ERK3 has been recently shown to play important roles in cancer cell proliferation, migration, invasion and chemoresistance in multiple types of cancers. Furthermore, accumulating studies have uncovered various molecular mechanisms by which the expression level, protein stability and activity of ERK3 are regulated. In particular, several post-translational modifications (PTMs), including ubiquitination, hydroxylation and phosphorylation, have been shown to regulate the stability and activity of ERK3 protein. In this review, we discuss recent findings regarding biochemical and cellular functions of ERK3, with a main focus on its roles in cancers, as well as the molecular mechanisms of regulating its expression and activity. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Cancer Metastasis)
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