New Insights into p53: A Powerful Gene’s Role in Cancer Therapy
Apr 22, 2025
Researchers reveal groundbreaking findings on the p53 gene, a key player in preventing cancer. This gene, known as the 'guardian of the genome', can halt harmful cell growth and even push damaged cells to self-destruct. New research in healthy cell models uncovers two promising therapeutic targets: ALDH3A1 and Nectin-4. These insights could revolutionize cancer therapy and address challenges faced by many treatments today.
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insights INSIGHT
Powerful Tumor Suppressor Role
The p53 gene acts as the body's natural defense by detecting DNA damage and stopping risky cell growth.
It either halts cell division or triggers self-destruction to prevent cancer mutations from spreading.
insights INSIGHT
Clean Cell Model Reveals p53
Studying p53 has been challenging due to mutations in cancer cell models that mask its true function.
Researchers used hTERT-RPE1, non-cancerous immortalized cells, to accurately observe p53 in near-normal conditions.
insights INSIGHT
Comprehensive p53 Cell Line Study
Researchers studied p53 in normal and mutated colorectal cancer cell lines, comparing gene expression with and without p53.
This dual approach allowed a comprehensive understanding of p53's tumor-suppressing effects.
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A new study from the Sidney Kimmel Comprehensive Cancer Center and Johns Hopkins University School of Medicine, published in Oncotarget, reveals that the gene p53, long known as the “guardian of the genome,” may be even more powerful than previously thought. By studying it in non-cancerous human cells, researchers discovered how p53 stops risky cell growth and uncovered two new potential targets for cancer therapy.
Understanding p53: The Genome’s Guardian Against Cancer
The p53 gene is one of the most important natural defenses our body has against cancer. When functioning properly, p53 detects damage in a cell’s DNA and either stops the cell from dividing or pushes it to self-destruct. This process helps prevent potentially dangerous mutations from spreading. However, many cancers find ways to silence or mutate p53, allowing uncontrolled growth and resistance to treatments.
Studying p53 in a clear and accurate way has long been a challenge. Most cancer cell models used in research already carry numerous genetic mutations, which can mask or alter how p53 truly functions. To fully understand this vital tumor-suppressing gene, scientists needed a model that closely resembled healthy, genetically stable human cells—yet could still be maintained and studied over time in the laboratory.
The Study: Exploring p53 in Normal and Cancer Cell Models
Researchers Jessica J. Miciak, Lucy Petrova, Rhythm Sajwan, Aditya Pandya, Mikayla Deckard, Andrew J. Munoz, and Fred Bunz explored p53 activity using a uniquely suitable cell line: hTERT-RPE1. These non-cancerous human cells are immortalized using telomerase, meaning they continue dividing like cancer cells, but without the chaotic mutations seen in tumors. This makes them an excellent model for studying how p53 operates in near-normal conditions.
Full blog - https://www.oncotarget.org/2025/04/22/new-insights-into-p53-a-powerful-genes-role-in-cancer-therapy/
Paper DOI - https://doi.org/10.18632/oncotarget.28690
Correspondence to - Fred Bunz - fredbunz@jhmi.edu
Video short - https://www.youtube.com/watch?v=Psxj3ctbTuk
Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28690
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Keywords - cancer, p53, ionizing radiation, immortalized cells, ALDH3A1, NECTIN4
About Oncotarget
Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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