Certain mammalian species are resistant to cancer, and a better understanding of how this cancer resistance arises could provide valuable insights for basic cancer research. Recent technological innovations in molecular biology have allowed the study of cancer-resistant mammals, despite the fact that they are not the classical model animals, which are easily studied using genetic approaches. Naked mole-rats (NMRs; Heterocephalus glaber) are the longest-lived rodent, with a maximum lifespan of more than 37 years, and almost never show spontaneous carcinogenesis. NMRs are currently attracting much attention from aging and cancer researchers, and published studies on NMR have continued to increase over the past decade. Cancer development occurs via multiple steps and involves many biological processes. Recent research on the NMR as a model for cancer resistance suggests that they possess various unique carcinogenesis-resistance mechanisms, including efficient DNA repair pathways, cell-autonomous resistance to transformation, and dampened inflammatory response. Here, we summarize the molecular mechanisms of carcinogenesis resistance in NMR, which have been uncovered over the past two decades, and discuss future perspectives.
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http://dx.doi.org/10.1111/cas.15570 | DOI Listing |
Metabol Open
March 2025
Department of Pharmaceutical Chemistry, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Manipal, 576104, Karnataka, India.
The highly nuanced transition from an inflammatory process to tumorigenesis is of great scientific interest. While it is well known that environmental stimuli can cause inflammation, less is known about the oncogenic modifications that chronic inflammation in the tissue microenvironment can bring about, as well as how these modifications can set off pro-tumorigenic processes. It is clear that no matter where the environmental factors come from, maintaining an inflammatory microenvironment encourages carcinogenesis.
View Article and Find Full Text PDFCancer Cell Int
January 2025
Department of Toxicology, Faculty of Medical Science, Tarbiat Modares University, Tehran, Iran.
Background: Cancer remains a leading cause of death worldwide. Environmental factors, specifically endocrine-disrupting chemicals (EDCs), like phthalates, are increasingly being linked to cancer development. Phthalates, widely used in consumer products, can activate the aryl hydrocarbon receptor (AhR).
View Article and Find Full Text PDFHeliyon
January 2025
Department of Cardiothoracic Surgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224002, China.
Research has demonstrated that POU3F4 is integral to various cancers, in addition to its significance in inner ear development, pancreatic differentiation, as well as neural stem cell differentiation. Nevertheless, comprehensive pan-cancer analyses focusing on POU3F4 remain limited. This study aims to assess the prognostic value of POU3F4 in thirty-three cancers and explore its immune-related functions.
View Article and Find Full Text PDFOncol Res
January 2025
College of Food Sciences, Al-Qasim Green University, Babylon, Iraq.
Cancer, a leading cause of global mortality, remains a significant challenge to increasing life expectancy worldwide. Forkhead Box R2 (FOXR2), identified as an oncogene within the FOX gene family, plays a crucial role in developing various endoderm-derived organs. Recent studies have elucidated FOXR2-related pathways and their involvement in both tumor and non-tumor diseases.
View Article and Find Full Text PDFAgeing Res Rev
January 2025
Zhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Hangzhou, Zhejiang 310022, China. Electronic address:
Protein lactylation, an emerging post-translational modification, is providing new insights into tumor biology and challenging our current understanding of cancer mechanisms. Our review illuminates the intricate roles of lactylation in carcinogenesis, tumor progression, and therapeutic responses, positioning it as a critical linchpin connecting metabolic reprogramming, epigenetic modulation, and treatment outcomes. We provide an in-depth analysis of lactylation's molecular mechanisms and its far-reaching impact on cell cycle regulation, immune evasion strategies, and therapeutic resistance within the complex tumor microenvironment.
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