Preprint Review Version 1 This version is not peer-reviewed

Exploring the Role of p53 in Radiosensitivity: A Key Player in Cancer Therapy

Version 1 : Received: 28 August 2024 / Approved: 29 August 2024 / Online: 29 August 2024 (12:07:42 CEST)

How to cite: -Al-Arafat, T.; Mao, A.; Katsube, T.; Wang, B. Exploring the Role of p53 in Radiosensitivity: A Key Player in Cancer Therapy. Preprints 2024, 2024082103. https://doi.org/10.20944/preprints202408.2103.v1 -Al-Arafat, T.; Mao, A.; Katsube, T.; Wang, B. Exploring the Role of p53 in Radiosensitivity: A Key Player in Cancer Therapy. Preprints 2024, 2024082103. https://doi.org/10.20944/preprints202408.2103.v1

Abstract

Radiotherapy remains a cornerstone in cancer treatment, leveraging ionizing radiation to eradicate malignant cells. Its efficacy, however, is frequently challenged by the heterogeneous sensitivity of tumors and surrounding tissues to radiation. Therefore, understanding the molecular mechanisms underlying radiosensitivity is crucial for improving treatment outcomes. Among the myriad of molecular players involved, the tumor suppressor protein p53 stands out as a central regulator with significant implications for radiosensitivity. Known as the “guardian of the genome,” p53 plays a pivotal role in maintaining genomic stability and orchestrating cellular responses such as cell cycle arrest, DNA repair, apoptosis, and senescence in response to various stress signals, including radiation-induced DNA damage. Activation of p53 triggers the transcription of target genes involved in DNA repair pathways, such as p21, MDM2, and GADD45, facilitating the repair of radiation-induced DNA damage or the elimination of irreparably damaged cells. This, in turn, influences the overall radiosensitivity of tissues. Mutations in the TP53 gene, which encodes p53, are among the most frequent genetic alterations in human cancers. Loss or dysfunction of p53 can compromise the cellular response to radiation, leading to increased resistance to therapy and poorer clinical outcomes. Conversely, intact p53 function is associated with enhanced radiosensitivity due to its ability to promote cell cycle arrest and apoptosis in response to radiation-induced DNA damage. In conclusion, elucidating the molecular mechanisms by which p53 influences radiosensitivity is essential for advancing our understanding of radiation response in cancer cells and developing more effective therapeutic approaches in cancer treatment. This review provides a comprehensive overview of the multifaceted role of p53 in modulating cellular responses to radiation, emphasizing its influence on radiosensitivity.

Keywords

radiation; p53; radiosensitivity; cancer therapy; DNA damage and repair; Apoptosis

Subject

Biology and Life Sciences, Biochemistry and Molecular Biology

Comments (0)

We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.

Leave a public comment
Send a private comment to the author(s)
* All users must log in before leaving a comment
Views 0
Downloads 0
Comments 0


×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.
We use cookies on our website to ensure you get the best experience.
Read more about our cookies here.