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Journals
Biomedicines
Special Issues
Regulators of Cancer Metastasis
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Regulators of Cancer Metastasis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 739

Special Issue Editors

Dr. Sanjib Chaudhary

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Guest Editor
Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA
Interests: lung cancer; HNSCC; animal model; therapeutics; metastasis
Dr. Julio C. Valencia

E-Mail Website
Guest Editor
Cancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA
Interests: immuno-oncology; immune-related toxicity; autoimmunity; targeted immunotherapy

Special Issue Information

Dear Colleagues,

Metastasis, the intricate process by which tumor cells spread from their primary site to distant organs, poses a critical challenge in cancer research. The journal Biomedicines is pleased to announce a forthcoming Special Issue focused on unraveling the multifaceted regulators that govern this complex phenomenon.

We invite scientists, clinicians, and researchers to contribute original research articles, comprehensive reviews, and insightful case studies that explore various facets of metastasis regulators. Topics of interest include, but are not limited to, the following:

  1. Epithelial–mesenchymal transition (EMT) and its pivotal role in initiating invasion and dissemination.
  2. Matrix metalloproteinases (MMPs) and their impact on extracellular matrix degradation during metastatic progression.
  3. Angiogenesis and lymphangiogenesis as facilitators of tumor vascularization and metastatic niche establishment.
  4. Cancer stem cells and their contribution to therapy resistance, tumor relapse, and metastatic potential.
  5. Immune system modulation of metastasis, encompassing both immune surveillance and immune cell promotion of spread.
  6. Impact of immunotherapy on metastasis response and toxicity.

Manuscripts will undergo a peer-review process, with accepted articles featured online in the Special Issue. This Special Issue serves as a platform to disseminate cutting-edge research and foster advancements in metastasis comprehension and intervention.

Dr. Sanjib Chaudhary
Dr. Julio C. Valencia
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. Biomedicines 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

  • metastasis
  • immune cells
  • cancer stem cells
  • therapy resistance
  • tumor progression

Published Papers (1 paper)

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Research

26 pages, 19943 KiB  
Article
GNPNAT1 Serves as a Prognostic Biomarker Correlated with Immune Infiltration and Promotes Cancer Cell Metastasis through Stabilization of Snai2 in Lung Adenocarcinoma
by Jinqi He, Faxiang Li, Zihan Jing, Xingmei Ren, Dexin Jia, Yuan Zeng and Yan Yu
Biomedicines 2024, 12(7), 1477; https://doi.org/10.3390/biomedicines12071477 - 4 Jul 2024
Viewed by 586
Abstract
Background: Lung cancer is a common malignant tumor with high morbidity and mortality rate. Glucosamine 6-phosphate N-acetyltransferase (GNPNAT1), which serves as a critical enzyme in hexosamine biosynthetic pathway (HBP), has been identified as a metastasis-associated gene and is upregulated in lung [...] Read more.
Background: Lung cancer is a common malignant tumor with high morbidity and mortality rate. Glucosamine 6-phosphate N-acetyltransferase (GNPNAT1), which serves as a critical enzyme in hexosamine biosynthetic pathway (HBP), has been identified as a metastasis-associated gene and is upregulated in lung adenocarcinoma (LUAD). However, the exact role and related mechanism of GNPNAT1 in LUAD metastasis remain unknown. Methods: We analyzed the expression of GNPNAT1 in the public databases and confirmed the results by immunohistochemistry (IHC). The biological functions of GNPNAT1 in LUAD were investigated based on The Cancer Genome Atlas (TCGA). Correlations between GNPNAT1 and cancer immune characteristics were analyzed via the Estimation of Stromal and Immune cells in Malignant Tumor tissues using Expression data (ESTIMATE) and Cell-type Identification by Estimating Relative Subsets of RNA Transcript (CIBERSORT) R package. The underlying mechanisms of altered GNPNAT1 expression on LUAD cell tumorigenesis, proliferation, migration, invasion, and metastasis were explored in vitro and in vivo. Results: We demonstrated that GNPNAT1 expression was significantly increased in LUAD and negatively associated with the overall survival (OS) of patients. hsa-miR-1-3p and hsa-miR-26a-5p were identified as upstream miRNA targets of GNPNAT1. GNPNAT1 was associated with the infiltration levels of CD8 T cells, memory-activated CD4 T cells, NK cells resting, macrophages M0, macrophages M1, neutrophils, gamma delta T cells, and eosinophils, while it was negatively correlated with memory-resting CD4 T cells, regulatory T cells (Tregs), resting NK cells, monocytes, resting dendritic cells, and resting mast cells. GNPNAT1 knockdown significantly inhibited proliferation, migration, invasion, epithelial–mesenchymal transition (EMT) process, and metastasis of LUAD cells, while overexpression of GNPNAT1 revealed the opposite effects. Rescue assay showed that Snai2 knockdown reversed GNPNAT1-induced LUAD cells migration, invasion, and EMT. Mechanistically, GNPNAT1 promoted cancer cell metastasis via repressing ubiquitination degradation of Snai2 in LUAD. Conclusions: Taken together, these data indicate that GNPNAT1 serves as a prognostic biomarker for LUAD patient. Additionally, GNPNAT1 is critical for promoting tumorigenesis and metastasis of LUAD cells and may be a potential therapeutic target for preventing LUAD metastasis. Full article
(This article belongs to the Special Issue Regulators of Cancer Metastasis)
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