Role of APR3 in cancer: apoptosis, autophagy, oxidative stress, and cancer therapy.

APR3 (Apoptosis-related protein 3) is a gene that has recently been identified to be associated with apoptosis. The gene is located on human chromosome 2p22.3 and contains both transmembrane and EGF (epidermal growth factor)-like domains. Additionally, it has structural sites, including AP1, SP1, and MEF2D, that indicate NFAT (nuclear factor of activated T cells) and NF-κB (nuclear factor kappa-B) may be transcription factors for this gene. Functionally, APR3 participates in apoptosis due to the induction of mitochondrial damage to release mitochondrial cytochrome C. Concurrently, APR3 affects the cell cycle by altering the expression of Cyclin D1, which, in turn, affects the incidence and growth of malignancies and promotes cell differentiation. Previous reports indicate that APR3 is located in lysosomal membranes, where it contributes to lysosomal activity and participates in autophagy. While further research is required to determine the precise role and molecular mechanisms of APR3, earlier studies have laid the groundwork for APR3 research. There is growing evidence supporting the significance of APR3 in oncology. Therefore, this review aims to examine the current state of knowledge on the role of the newly discovered APR3 in tumorigenesis and to generate fresh insights and suggestions for future research. Highlight: 1. APR3-mediated mitochondrial damage plays a vital function in oxidative stress and apoptosis. 2. APR3 is discovered as an apoptosis-related gene and participated in cell cycle and cellular homeostasis. 3. The rivalry between NFAT and NF-κB for the binding domains of APR3 can have an impact on its transcription. 4. The expression of APR3 is increased in tumor tissues, which is expected to be an emerging disease biomarker and therapeutic target. 5. APR3 may have an integral role in nonapoptotic programmed cell death, such as autophagy, ferroptosis, cuproptosis, and pyroptosis. [ABSTRACT FROM AUTHOR]