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Tumorigenesis and Tumor Microenvironment
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Tumorigenesis and Tumor Microenvironment

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: 10 April 2025 | Viewed by 5558

Special Issue Editor

Dr. Yaser Gamallat

E-Mail Website
Guest Editor
Department of Pathology and Laboratory Medicine, Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada
Interests: prostate cancer; genomics; transcriptome; tumor biomarkers; tumorigenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In this special issue, we seek articles and reviews that bring new insight advancing our understanding of Tumorigenesis and Tumor Microenvironment and bring together diverse perspectives and groundbreaking discoveries in the field. We invite researchers to submit articles and reviews with focus on emerging therapies, targeting the tumor microenvironment, and molecular pathways of tumorigenesis, with the aim to develop biomarkers, or early diagnostics or effective cancer treatments including, the role of immune cells, stromal cells, extracellular matrix, and signaling pathways in promoting or inhibiting tumor growth, progression, and metastasis are the target for this special issue.

Dr. Yaser Gamallat
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. Current Issues in Molecular Biology 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 2200 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
  • tumor growth
  • tumor progression
  • tumor metastasis
  • cancers

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Published Papers (4 papers)

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Research

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10 pages, 8024 KiB  
Article
Knockdown of Gas6 Exerts Anti-Esophageal Cancer Effects by Inhibiting the PI3K/AKT Pathway
by Shuang Gao, Yu Wang, Ming Huang, Jianxin Guo, Zhongbing Wu and Jing Li
Curr. Issues Mol. Biol. 2024, 46(10), 11349-11358; https://doi.org/10.3390/cimb46100676 - 13 Oct 2024
Viewed by 593
Abstract
Esophageal squamous cell carcinoma (ESCC) is a malignant tumor of the digestive tract with strong migratory and invasive abilities. Gas6 is closely associated with the progression of many malignant tumors; however, the role of Gas6 in the progression of esophageal cancer is unclear. [...] Read more.
Esophageal squamous cell carcinoma (ESCC) is a malignant tumor of the digestive tract with strong migratory and invasive abilities. Gas6 is closely associated with the progression of many malignant tumors; however, the role of Gas6 in the progression of esophageal cancer is unclear. Here, we report that the knockdown of Gas6 inhibited esophageal cancer cell proliferation, migration, and invasion. In addition, Gas6 knockdown downregulated the levels of P-PI3K and P-AKT. Taken together, the findings confirm that Gas6 knockdown can inhibit esophageal cancer progression and can exert anti-tumor effects on esophageal cancer through the PI3K/AKT pathway. Full article
(This article belongs to the Special Issue Tumorigenesis and Tumor Microenvironment)
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24 pages, 9653 KiB  
Article
Bioinformatics Analysis Reveals E6 and E7 of HPV 16 Regulate Metabolic Reprogramming in Cervical Cancer, Head and Neck Cancer, and Colorectal Cancer through the PHD2-VHL-CUL2-ELOC-HIF-1α Axis
by Adán Arizmendi-Izazaga, Napoleón Navarro-Tito, Hilda Jiménez-Wences, Adilene Evaristo-Priego, Víctor Daniel Priego-Hernández, Roberto Dircio-Maldonado, Ana Elvira Zacapala-Gómez, Miguel Ángel Mendoza-Catalán, Berenice Illades-Aguiar, Mónica Ascención De Nova Ocampo, Eric Genaro Salmerón-Bárcenas, Marco Antonio Leyva-Vázquez and Julio Ortiz-Ortiz
Curr. Issues Mol. Biol. 2024, 46(6), 6199-6222; https://doi.org/10.3390/cimb46060370 - 19 Jun 2024
Viewed by 1447
Abstract
Human papillomavirus 16 (HPV 16) infection is associated with several types of cancer, such as head and neck, cervical, anal, and penile cancer. Its oncogenic potential is due to the ability of the E6 and E7 oncoproteins to promote alterations associated with cell [...] Read more.
Human papillomavirus 16 (HPV 16) infection is associated with several types of cancer, such as head and neck, cervical, anal, and penile cancer. Its oncogenic potential is due to the ability of the E6 and E7 oncoproteins to promote alterations associated with cell transformation. HPV 16 E6 and E7 oncoproteins increase metabolic reprogramming, one of the hallmarks of cancer, by increasing the stability of hypoxia-induced factor 1 α (HIF-1α) and consequently increasing the expression levels of their target genes. In this report, by bioinformatic analysis, we show the possible effect of HPV 16 oncoproteins E6 and E7 on metabolic reprogramming in cancer through the E6-E7-PHD2-VHL-CUL2-ELOC-HIF-1α axis. We proposed that E6 and E7 interact with VHL, CUL2, and ELOC in forming the E3 ubiquitin ligase complex that ubiquitinates HIF-1α for degradation via the proteasome. Based on the information found in the databases, it is proposed that E6 interacts with VHL by blocking its interaction with HIF-1α. On the other hand, E7 interacts with CUL2 and ELOC, preventing their binding to VHL and RBX1, respectively. Consequently, HIF-1α is stabilized and binds with HIF-1β to form the active HIF1 complex that binds to hypoxia response elements (HREs), allowing the expression of genes related to energy metabolism. In addition, we suggest an effect of E6 and E7 at the level of PHD2, VHL, CUL2, and ELOC gene expression. Here, we propose some miRNAs targeting PHD2, VHL, CUL2, and ELOC mRNAs. The effect of E6 and E7 may be the non-hydroxylation and non-ubiquitination of HIF-1α, which may regulate metabolic processes involved in metabolic reprogramming in cancer upon stabilization, non-degradation, and translocation to the nucleus. Full article
(This article belongs to the Special Issue Tumorigenesis and Tumor Microenvironment)
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Review

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28 pages, 4477 KiB  
Review
Advancements in Understanding the Hide-and-Seek Strategy of Hibernating Breast Cancer Cells and Their Implications in Oncology from a Broader Perspective: A Comprehensive Overview
by Aiman Al-Ruwishan, Bushra Amer, Ahmed Salem, Ahmed Abdi, Namoonga Chimpandu, Abdelmonem Esa, Alexandros Melemenis, Muhammad Zubair Saleem, Roselit Mathew and Yaser Gamallat
Curr. Issues Mol. Biol. 2024, 46(8), 8340-8367; https://doi.org/10.3390/cimb46080492 - 1 Aug 2024
Viewed by 1104
Abstract
Despite recent advancements in technology, breast cancer still poses a significant threat, often resulting in fatal consequences. While early detection and treatments have shown some promise, many breast cancer patients continue to struggle with the persistent fear of the disease returning. This fear [...] Read more.
Despite recent advancements in technology, breast cancer still poses a significant threat, often resulting in fatal consequences. While early detection and treatments have shown some promise, many breast cancer patients continue to struggle with the persistent fear of the disease returning. This fear is valid, as breast cancer cells can lay dormant for years before remerging, evading traditional treatments like a game of hide and seek. The biology of these dormant breast cancer cells presents a crucial yet poorly understood challenge in clinical settings. In this review, we aim to explore the mysterious world of dormant breast cancer cells and their significant impact on patient outcomes and prognosis. We shed light on the elusive role of the G9a enzyme and many other epigenetic factors in breast cancer recurrence, highlighting its potential as a target for eliminating dormant cancer cells and preventing disease relapse. Through this comprehensive review, we not only emphasise the urgency of unravelling the dynamics of dormant breast cancer cells to improve patient outcomes and advance personalised oncology but also provide a guide for fellow researchers. By clearly outlining the clinical and research gaps surrounding dormant breast cancer cells from a molecular perspective, we aim to inspire further exploration of this critical area, ultimately leading to improved patient care and treatment strategies. Full article
(This article belongs to the Special Issue Tumorigenesis and Tumor Microenvironment)
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19 pages, 6816 KiB  
Review
MASLD-Related HCC: A Comprehensive Review of the Trends, Pathophysiology, Tumor Microenvironment, Surveillance, and Treatment Options
by Yuming Shi, Erfan Taherifard, Ali Saeed and Anwaar Saeed
Curr. Issues Mol. Biol. 2024, 46(6), 5965-5983; https://doi.org/10.3390/cimb46060356 - 13 Jun 2024
Cited by 4 | Viewed by 1788
Abstract
Hepatocellular carcinoma (HCC) represents a significant burden on global healthcare systems due to its considerable incidence and mortality rates. Recent trends indicate an increase in the worldwide incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) and a shift in the etiology of HCC, [...] Read more.
Hepatocellular carcinoma (HCC) represents a significant burden on global healthcare systems due to its considerable incidence and mortality rates. Recent trends indicate an increase in the worldwide incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) and a shift in the etiology of HCC, with MASLD replacing the hepatitis B virus as the primary contributor to new cases of HCC. MASLD-related HCC exhibits distinct characteristics compared to viral HCC, including unique immune cell profiles resulting in an overall more immunosuppressive or exhausted tumor microenvironment. Furthermore, MASLD-related HCC is frequently identified in older age groups and among individuals with cardiometabolic comorbidities. Additionally, a greater percentage of MASLD-related HCC cases occur in noncirrhotic patients compared to those with viral etiologies, hindering early detection. However, the current clinical practice guidelines lack specific recommendations for the screening of HCC in MASLD patients. The evolving landscape of HCC management offers a spectrum of therapeutic options, ranging from surgical interventions and locoregional therapies to systemic treatments, for patients across various stages of the disease. Despite ongoing debates, the current evidence does not support differences in optimal treatment modalities based on etiology. In this study, we aimed to provide a comprehensive overview of the current literature on the trends, characteristics, clinical implications, and treatment modalities for MASLD-related HCC. Full article
(This article belongs to the Special Issue Tumorigenesis and Tumor Microenvironment)
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