Targeting Hallmarks of Cancer

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 25 April 2025 | Viewed by 692

Special Issue Editor


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Guest Editor
1. Laboratorio de Genómica, Instituto Nacional de Cancerología, Tlalpan 14080, México
2. Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla 54090, Mexico
Interests: microRNAs; lncRNAs; cancer genomics; transcriptomics
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Special Issue Information

Dear Colleagues,

Cancer remains one of the most significant challenges in modern medicine, characterized by its complexity, heterogeneity, and ability to evolve rapidly. The pursuit of new, efficient drugs to combat cancer is a top priority in biomedical research. However, the development of such therapies is not a straightforward process. It requires a deep understanding of the fundamental mechanisms driving cancer progression, including the hallmark traits of cancer cells and the intricate signaling pathways involved in maintaining the tumor phenotype. In this context, the creation and utilization of biological models, such as organotypic cell cultures, and the study of epigenetic regulators, like long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are crucial for advancing our ability to develop effective anti-cancer drugs.

The quest to develop new, efficient drugs to fight cancer is intrinsically linked to our understanding of the biological processes that underlie the disease. Biological models, from simple cell cultures to sophisticated animal models and organoids, are indispensable tools for studying the hallmarks of cancer and the signaling pathways that define the tumor phenotype. Additionally, the exploration of epigenetic regulators, such as lncRNAs and miRNAs, opens up new possibilities for targeted therapies that could complement existing treatments. As research in these areas continues to advance, it brings us closer to realizing the goal of developing more effective and personalized cancer therapies, ultimately improving outcomes for patients worldwide.

You may choose our Joint Special Issue in Cancers.

Prof. Dr. Carlos Pérez Plasencia
Guest Editor

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Keywords

  • epigenetic regulators
  • organotypic culture models
  • anticancer drugs
  • hallmarks of cancer

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Published Papers (1 paper)

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Research

21 pages, 8382 KiB  
Article
Laherradurin Inhibits Colorectal Cancer Cell Growth by Induction of Mitochondrial Dysfunction and Autophagy Induction
by Izamary Delgado-Waldo, Svetlana Dokudovskaya, Yahir A. Loissell-Baltazar, Eduardo Pérez-Arteaga, Jossimar Coronel-Hernández, Mariano Martínez-Vázquez, Eloy Andrés Pérez-Yépez, Alejandro Lopez-Saavedra, Nadia Jacobo-Herrera and Carlos Pérez Plasencia
Cells 2024, 13(19), 1649; https://doi.org/10.3390/cells13191649 - 3 Oct 2024
Abstract
LAH, an acetogenin from the Annonaceae family, has demonstrated antitumor activity in several cancer cell lines and in vivo models, where it reduced the tumor size and induced programmed cell death. We focused on the effects of LAH on mitochondrial dynamics, mTOR signaling, [...] Read more.
LAH, an acetogenin from the Annonaceae family, has demonstrated antitumor activity in several cancer cell lines and in vivo models, where it reduced the tumor size and induced programmed cell death. We focused on the effects of LAH on mitochondrial dynamics, mTOR signaling, autophagy, and apoptosis in colorectal cancer (CRC) cells to explore its anticancer potential. Methods: CRC cells were treated with LAH, and its effects on mitochondrial respiration and glycolysis were measured using Seahorse XF technology. The changes in mitochondrial dynamics were observed through fluorescent imaging, while Western blot analysis was used to examine key autophagy and apoptosis markers. Results: LAH significantly inhibited mitochondrial complex I activity, inducing ATP depletion and a compensatory increase in glycolysis. This disruption caused mitochondrial fragmentation, a trigger for autophagy, as shown by increased LC3-II expression and mTOR suppression. Apoptosis was also confirmed through the cleavage of caspase-3, contributing to reduced cancer cell viability. Conclusions: LAH’s anticancer effects in CRC cells are driven by its disruption of mitochondrial function, triggering both autophagy and apoptosis. These findings highlight its potential as a therapeutic compound for further exploration in cancer treatment. Full article
(This article belongs to the Special Issue Targeting Hallmarks of Cancer)
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