Crosslink between p53 and metastasis: focus on epithelial-mesenchymal transition, cancer stem cell, angiogenesis, autophagy, and anoikis

Introduction P53, as a tumor suppressor gene, is believed to be one of the most mutated genes in cancer cells. The mutant forms of this protein often play a tumorigenic role in cancer cells. Recent evidence shows that p53 plays a critical role in the migration, metastasis, and invasion of cancer cells. The present article aims to investigate the molecular mechanism that induces metastasis in cancer cells generated by the mutant P53, and to highlight the compounds targeting mutant-p53 together with their clinical applications. Methods A detailed literature search was conducted to find information about the role of the mutant-p53 in the processes involved in metastasis in various databases. Results A growing body of evidence suggests that Mutant-p53 enhances tumor metastasis affecting the Epithelial-mesenchymal transition (EMT) process, cancer stem cells, angiogenesis, autophagy, anoikis, and any other mechanisms regarding metastasis. Conclusions Taken together, targeting mutant-p53 by altering the processes involved in metastasis could be a potential therapeutic strategy in the treatment of metastatic cancer. [GRAPHICS]

Automated summary

Mutant P53 plays a critical role in tumor metastasis by enhancing the processes like epithelial-mesenchymal transition (EMT), cancer stem cells, angiogenesis, autophagy, anoikis, and other mechanisms related to metastasis. Targeting mutant-p53 may be a potential therapeutic strategy in the treatment of metastatic cancer.