Mutant p53 is a key player in cancer progression, often resulting from TP53 mutations that lead to the expression of dysfunctional p53 proteins. These mutant p53 proteins not only lose their tumor suppressor function but also gain oncogenic properties, contributing to malignant transformation. Understanding the functions of mutant p53 is crucial for developing new therapeutic strategies for various cancers. p53, a well-known tumor suppressor, has been reclassified as an oncoprotein in some cases due to its mutant forms. Recent studies highlight that mutant p53 can promote tumor growth, metastasis, and resistance to therapy. Mutant p53 can interact with other proteins, leading to genomic instability, chemoresistance, and enhanced cell survival. It can also regulate gene expression through interactions with transcription factors like TAp63, promoting invasive and metastatic behavior. Mutant p53 can also influence the tumor microenvironment, including stromal cells, by promoting inflammation and enhancing tumor growth. Therapeutic strategies to target mutant p53 include restoring wild-type p53 function, promoting its degradation, and inhibiting its interactions with other proteins. Small molecules like PRIMA-1 and compounds that stabilize p53 structure have shown promise in restoring wild-type p53 function. Additionally, HDAC inhibitors and autophagy-inducing agents can destabilize mutant p53. Targeting mutant p53-regulated pathways, such as cholesterol synthesis and receptor tyrosine kinase signaling, is another approach. Despite these advances, challenges remain in translating mutant p53 research into clinical applications. The diversity of mutant p53 proteins and their varying effects on tumor biology require further investigation. Future directions include exploring synthetic lethality and leveraging computational approaches to identify potential therapeutic targets. Overall, understanding the complex functions of mutant p53 and developing effective therapies to target these proteins hold significant promise for improving cancer treatment.Mutant p53 is a key player in cancer progression, often resulting from TP53 mutations that lead to the expression of dysfunctional p53 proteins. These mutant p53 proteins not only lose their tumor suppressor function but also gain oncogenic properties, contributing to malignant transformation. Understanding the functions of mutant p53 is crucial for developing new therapeutic strategies for various cancers. p53, a well-known tumor suppressor, has been reclassified as an oncoprotein in some cases due to its mutant forms. Recent studies highlight that mutant p53 can promote tumor growth, metastasis, and resistance to therapy. Mutant p53 can interact with other proteins, leading to genomic instability, chemoresistance, and enhanced cell survival. It can also regulate gene expression through interactions with transcription factors like TAp63, promoting invasive and metastatic behavior. Mutant p53 can also influence the tumor microenvironment, including stromal cells, by promoting inflammation and enhancing tumor growth. Therapeutic strategies to target mutant p53 include restoring wild-type p53 function, promoting its degradation, and inhibiting its interactions with other proteins. Small molecules like PRIMA-1 and compounds that stabilize p53 structure have shown promise in restoring wild-type p53 function. Additionally, HDAC inhibitors and autophagy-inducing agents can destabilize mutant p53. Targeting mutant p53-regulated pathways, such as cholesterol synthesis and receptor tyrosine kinase signaling, is another approach. Despite these advances, challenges remain in translating mutant p53 research into clinical applications. The diversity of mutant p53 proteins and their varying effects on tumor biology require further investigation. Future directions include exploring synthetic lethality and leveraging computational approaches to identify potential therapeutic targets. Overall, understanding the complex functions of mutant p53 and developing effective therapies to target these proteins hold significant promise for improving cancer treatment.