Ghader Babaei1,2, Azadeh Aliarab3, Mehdi Asghari Vostakolaei4, Masumeh Hotelchi3, Roghaiyeh Neisari5, Shiva Gholizadeh-Ghaleh Aziz6, Masumeh Rajabi Bazl7. 1. Department of Biochemistry, Faculty of Medicine, Urmia Medical Sciences University (UMSU), Urmia, Iran. 2. Student Research Committee, Urmia Medical Sciences University, Urmia, Iran. 3. Department of Clinical Biochemistry, Faculty of Medicine, Shahid Beheshti University of Medical Sciences(SBUMS), Tehran, Iran. 4. Digestive Diseases Research Center, Ardabil University of Medical Sciences, Ardabil, Iran. 5. Shahid Motahhari Hospital, Urmia University of Medical Science, Urmia, Iran. 6. Department of Biochemistry, Faculty of Medicine, Urmia Medical Sciences University (UMSU), Urmia, Iran. gholizadeh.sh@umsu.ac.ir. 7. Department of Clinical Biochemistry, Faculty of Medicine, Shahid Beheshti University of Medical Sciences(SBUMS), Tehran, Iran. rajabi_m@sbmu.ac.ir.
Abstract
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.
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.
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