Peran APR-246 dalam Mengaktivasi P53 yang Berkaitan dengan Sensitivitas terhadap Respon Radioterapi: Studi Literatur

Annisa Fauzia; Septelia Inawati Wanandi; Fielda Djuita

doi:10.55451/jri.v8i1.382

Annisa Fauzia Universitas Indonesia
Septelia Inawati Wanandi Department of Biochemistry and Molecular Biology, Faculty of Medicine, Universitas Indonesia, Indonesia
Fielda Djuita Radiotherapy Department, Dharmais National Cancer Hospital, Indonesia

DOI: https://doi.org/10.55451/jri.v8i1.382

Keywords: APR-246, Radiotherapy, Radioresistant, P53

Abstract

Background: Cancer is a significant challenge to life expectancy globally. The main treatment modalities for cancer include chemotherapy, surgery, and radiotherapy. Radiotherapy targets only the affected body area, treatment directly targets cancer cells. Despite significant advancements in understanding the molecular mechanisms of carcinogenesis and the development of modern radiotherapy techniques, treatment effectiveness can vary due to factors like radioresistance. One of the key processes responsible for this radioresistance is the effectiveness of DNA damage repair following radiation exposure.

Methods: This study is a narrative review based on articles from PubMed, ClinicalKey, and ScienceDirect, covering the period from 2014 to 2024. To support the theoretical framework, earlier publications before 2014 were also reviewed.

Results: APR-246 (PRIMA-1MET) is a compound capable of restoring the wild-type conformation of p53 and its anti-tumor transcriptional activity by covalently binding to the DNA-binding domain of mutant p53. APR-246 functions as a radiosensitizer by inducing apoptosis and is known for activating and stabilizing the p53 protein.

Conclusion: The induction of apoptosis by the compound APR-246 through p53 activity can trigger a cellular response to radiation-induced stress, thereby facilitating the elimination of genetically damaged cancer cells and ultimately enhancing the response to radiotherapy.