Cellular and Molecular Dysregulations of Solid Tumors

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 1786

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Molecular Imaging Program at Stanford, Department of Radiology, Stanford University, Stanford, CA 94305, USA
Interests: molecular oncology; immunotherapy
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Special Issue Information

Dear Colleagues,

Cancer continues to take a toll on global public health systems, accounting for an estimated 8.7 million deaths annually. In 2015, 17.5 million incident cases were diagnosed worldwide, and this is projected to spiral to 22.2 million by 2030.

Despite tremendous progress in reducing mortality rates from cancer and transformative shifts in therapeutic paradigms over the past few years, investigation of the molecular and cellular aspects of solid tumor remains an urgent priority.

Solid tumors commonly arise from genetic mutations in driver oncogenes and tumor suppressor genes that have profound consequences on cell differentiation, proliferation, survival, and genomic stability. During cancer progression, tumor cells alter normal developmental processes to orchestrate a supportive but overtly immunosuppressive tumor microenvironment (TME) comprised of immune cells, fibroblasts, and endothelial cells, often embedded within a robust extracellular matrix (ECM). Characterizing the complex composition of cellular and molecular aspects of solid tumors is fundamental for understanding tumor initiation, progression and metastasis. In this Special Issue, we invite investigators to contribute original research or review articles that highlight recent important advances in cellular and molecular dysregulations of solid tumors. Potential topics include but are not limited to the following:

  • Genomic and proteomic characteristics of solid tumors
  • Tumor microenvironment and its role in tumor development, growth, and metastasis
  • Cancer stem cells and their roles in tumor development, drug resistance, and metastasis
  • Dysregulation of signaling pathways and their role in promoting cancer and drug resistance
  • Novel mechanisms underlying tumor development

Dr. Raheleh Roudi
Guest Editor

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Keywords

  • solid tumors
  • signaling pathways
  • genetic dysregulations
  • cellular abnormalities
  • cancer treatment

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Published Papers (1 paper)

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Research

20 pages, 11325 KiB  
Article
Pirfenidone Reverts Global DNA Hypomethylation, Promoting DNMT1/UHRF/PCNA Coupling Complex in Experimental Hepatocarcinoma
by Hipolito Otoniel Miranda-Roblero, Liliana Faridi Saavedra-Salazar, Marina Galicia-Moreno, Scarlet Arceo-Orozco, Fernando Caloca-Camarena, Ana Sandoval-Rodriguez, Jesús García-Bañuelos, Claudia Frias-Gonzalez, Mónica Almeida-López, Erika Martínez-López, Juan Armendariz-Borunda and Hugo Christian Monroy-Ramirez
Cells 2024, 13(12), 1013; https://doi.org/10.3390/cells13121013 - 10 Jun 2024
Cited by 1 | Viewed by 1182
Abstract
Hepatocellular carcinoma (HCC) development is associated with altered modifications in DNA methylation, changing transcriptional regulation. Emerging evidence indicates that DNA methyltransferase 1 (DNMT1) plays a key role in the carcinogenesis process. This study aimed to investigate how pirfenidone (PFD) modifies this pathway and [...] Read more.
Hepatocellular carcinoma (HCC) development is associated with altered modifications in DNA methylation, changing transcriptional regulation. Emerging evidence indicates that DNA methyltransferase 1 (DNMT1) plays a key role in the carcinogenesis process. This study aimed to investigate how pirfenidone (PFD) modifies this pathway and the effect generated by the association between c-Myc expression and DNMT1 activation. Rats F344 were used for HCC development using 50 mg/kg of diethylnitrosamine (DEN) and 25 mg/kg of 2-Acetylaminofluorene (2-AAF). The HCC/PFD group received simultaneous doses of 300 mg/kg of PFD. All treatments lasted 12 weeks. On the other hand, HepG2 cells were used to evaluate the effects of PFD in restoring DNA methylation in the presence of the inhibitor 5-Aza. Histopathological, biochemical, immunohistochemical, and western blot analysis were carried out and our findings showed that PFD treatment reduced the amount and size of tumors along with decreased Glipican-3, β-catenin, and c-Myc expression in nuclear fractions. Also, this treatment improved lipid metabolism by modulating PPARγ and SREBP1 signaling. Interestingly, PFD augmented DNMT1 and DNMT3a protein expression, which restores global methylation, both in our in vivo and in vitro models. In conclusion, our results suggest that PFD could slow down HCC development by controlling DNA methylation. Full article
(This article belongs to the Special Issue Cellular and Molecular Dysregulations of Solid Tumors)
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