Unraveling the Oncogenic Potential of VAV1 in Human Cancer: Lessons from Mouse Models
VAV1 is a hematopoietic signal transducer that possesses a GDP/GTP nucleotide exchange factor (GEF) that is tightly regulated by tyrosine phosphorylation, along with adapter protein domains, such as SH2 and SH3. Research on <i>VAV1</i> has advanced over the years since its discovery as a...
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| Format: | Article |
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MDPI AG
2023-04-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/12/9/1276 |
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| author | Batel Shalom Yaser Salaymeh Matan Risling Shulamit Katzav |
| author_facet | Batel Shalom Yaser Salaymeh Matan Risling Shulamit Katzav |
| author_sort | Batel Shalom |
| collection | DOAJ |
| description | VAV1 is a hematopoietic signal transducer that possesses a GDP/GTP nucleotide exchange factor (GEF) that is tightly regulated by tyrosine phosphorylation, along with adapter protein domains, such as SH2 and SH3. Research on <i>VAV1</i> has advanced over the years since its discovery as an in vitro activated oncogene in an NIH3T3 screen for oncogenes. Although the oncogenic form of <i>VAV1</i> first identified in the screen has not been detected in human clinical tumors, its wild-type and mutant forms have been implicated in mammalian malignancies of various tissue origins, as well as those of the hematopoietic system. This review article addresses the activity of human <i>VAV1</i> as an overexpressed or mutated gene and also describes the differences in the distribution of <i>VAV1</i> mutations in the hematopoietic system and in other tissues. The knowledge accumulated thus far from GEMMs expressing <i>VAV1</i> is described, with the conclusion that GEMMs of both wild-type <i>VAV1</i> and mutant <i>VAV1</i> do not form tumors, yet these will be generated when additional molecular insults, such as loss of p53 or KRAS mutation, occur. |
| first_indexed | 2024-03-11T04:22:46Z |
| format | Article |
| id | doaj.art-f80357afccb44046933feaffceda3c93 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-11T04:22:46Z |
| publishDate | 2023-04-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-f80357afccb44046933feaffceda3c932023-11-17T22:43:42ZengMDPI AGCells2073-44092023-04-01129127610.3390/cells12091276Unraveling the Oncogenic Potential of VAV1 in Human Cancer: Lessons from Mouse ModelsBatel Shalom0Yaser Salaymeh1Matan Risling2Shulamit Katzav3Department of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Faculty of Medicine, Hebrew University, Jerusalem 91120, IsraelDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Faculty of Medicine, Hebrew University, Jerusalem 91120, IsraelDepartment of Military Medicine and “Tzameret”, Faculty of Medicine, Hebrew University, Jerusalem 91120, IsraelDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Faculty of Medicine, Hebrew University, Jerusalem 91120, IsraelVAV1 is a hematopoietic signal transducer that possesses a GDP/GTP nucleotide exchange factor (GEF) that is tightly regulated by tyrosine phosphorylation, along with adapter protein domains, such as SH2 and SH3. Research on <i>VAV1</i> has advanced over the years since its discovery as an in vitro activated oncogene in an NIH3T3 screen for oncogenes. Although the oncogenic form of <i>VAV1</i> first identified in the screen has not been detected in human clinical tumors, its wild-type and mutant forms have been implicated in mammalian malignancies of various tissue origins, as well as those of the hematopoietic system. This review article addresses the activity of human <i>VAV1</i> as an overexpressed or mutated gene and also describes the differences in the distribution of <i>VAV1</i> mutations in the hematopoietic system and in other tissues. The knowledge accumulated thus far from GEMMs expressing <i>VAV1</i> is described, with the conclusion that GEMMs of both wild-type <i>VAV1</i> and mutant <i>VAV1</i> do not form tumors, yet these will be generated when additional molecular insults, such as loss of p53 or KRAS mutation, occur.https://www.mdpi.com/2073-4409/12/9/1276VAV1GEMMsKRASp53RAC1 |
| spellingShingle | Batel Shalom Yaser Salaymeh Matan Risling Shulamit Katzav Unraveling the Oncogenic Potential of VAV1 in Human Cancer: Lessons from Mouse Models Cells VAV1 GEMMs KRAS p53 RAC1 |
| title | Unraveling the Oncogenic Potential of VAV1 in Human Cancer: Lessons from Mouse Models |
| title_full | Unraveling the Oncogenic Potential of VAV1 in Human Cancer: Lessons from Mouse Models |
| title_fullStr | Unraveling the Oncogenic Potential of VAV1 in Human Cancer: Lessons from Mouse Models |
| title_full_unstemmed | Unraveling the Oncogenic Potential of VAV1 in Human Cancer: Lessons from Mouse Models |
| title_short | Unraveling the Oncogenic Potential of VAV1 in Human Cancer: Lessons from Mouse Models |
| title_sort | unraveling the oncogenic potential of vav1 in human cancer lessons from mouse models |
| topic | VAV1 GEMMs KRAS p53 RAC1 |
| url | https://www.mdpi.com/2073-4409/12/9/1276 |
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