RUNX1 and its understudied role in breast cancer
The transcription factor Runt-related transcription factor 1 (RUNX1) is critical for the earliest steps of hematopoiesis. RUNX1 was originally identified as a gene fusion in acute myeloid leukemia (AML) and thus has garnered heavy attention as a tumor suppressor in hematopoietic malignancies. Howeve...
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| Published in | Cell cycle (Georgetown, Tex.) Vol. 10; no. 20; pp. 3461 - 3465 |
|---|---|
| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
United States
Taylor & Francis
15.10.2011
Landes Bioscience |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1538-4101 1551-4005 1551-4005 |
| DOI | 10.4161/cc.10.20.18029 |
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| Abstract | The transcription factor Runt-related transcription factor 1 (RUNX1) is critical for the earliest steps of hematopoiesis. RUNX1 was originally identified as a gene fusion in acute myeloid leukemia (AML) and thus has garnered heavy attention as a tumor suppressor in hematopoietic malignancies. However, RUNX1 is also strongly expressed in breast epithelia and may be misregulated during tumorigenesis. Here, I discuss our recent work implicating RUNX1 in proliferation control during breast epithelial-acinar morphogenesis. My goal is to place these findings in the context of a handful of other reports, which together argue that RUNX1 could act as a tumor suppressor gene in breast cancer. Testing this hypothesis requires focused in vivo studies, because the major commercial platform for global mRNA expression profiling does not reliably reflect RUNX1 levels. Our in vitro results indicate that hyperproliferation in RUNX1-deficient breast epithelia relies on another family of transcription factors, the Forkhead box O (FOXO) proteins. FOXOs could, therefore, represent a synthetic-lethal target for RUNX1-deficient tumors if the hypothesized link to breast cancer is correct. |
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| AbstractList | The transcription factor Runt-related transcription factor 1 (RUNX1) is critical for the earliest steps of hematopoiesis. RUNX1 was originally identified as a gene fusion in acute myeloid leukemia (AML) and thus has garnered heavy attention as a tumor suppressor in hematopoietic malignancies. However, RUNX1 is also strongly expressed in breast epithelia and may be misregulated during tumorigenesis. Here, I discuss our recent work implicating RUNX1 in proliferation control during breast epithelial-acinar morphogenesis. My goal is to place these findings in the context of a handful of other reports, which together argue that RUNX1 could act as a tumor suppressor gene in breast cancer. Testing this hypothesis requires focused in vivo studies, because the major commercial platform for global mRNA expression profiling does not reliably reflect RUNX1 levels. Our in vitro results indicate that hyperproliferation in RUNX1-deficient breast epithelia relies on another family of transcription factors, the Forkhead box O (FOXO) proteins. FOXOs could, therefore, represent a synthetic-lethal target for RUNX1-deficient tumors if the hypothesized link to breast cancer is correct. The transcription factor Runt-related transcription factor 1 (RUNX1) is critical for the earliest steps of hematopoiesis. RUNX1 was originally identified as a gene fusion in acute myeloid leukemia (AML) and thus has garnered heavy attention as a tumor suppressor in hematopoietic malignancies. However, RUNX1 is also strongly expressed in breast epithelia and may be misregulated during tumorigenesis. Here, I discuss our recent work implicating RUNX1 in proliferation control during breast epithelial-acinar morphogenesis. My goal is to place these findings in the context of a handful of other reports, which together argue that RUNX1 could act as a tumor suppressor gene in breast cancer. Testing this hypothesis requires focused in vivo studies, because the major commercial platform for global mRNA expression profiling does not reliably reflect RUNX1 levels. Our in vitro results indicate that hyperproliferation in RUNX1-deficient breast epithelia relies on another family of transcription factors, the Forkhead box O (FOXO) proteins. FOXOs could, therefore, represent a synthetic-lethal target for RUNX1-deficient tumors if the hypothesized link to breast cancer is correct. The transcription factor Runt-related transcription factor 1 (RUNX1) is critical for the earliest steps of hematopoiesis. RUNX1 was originally identified as a gene fusion in acute myeloid leukemia (AML) and thus has garnered heavy attention as a tumor suppressor in hematopoietic malignancies. However, RUNX1 is also strongly expressed in breast epithelia and may be misregulated during tumorigenesis. Here, I discuss our recent work implicating RUNX1 in proliferation control during breast epithelial-acinar morphogenesis. My goal is to place these findings in the context of a handful of other reports, which together argue that RUNX1 could act as a tumor suppressor gene in breast cancer. Testing this hypothesis requires focused in vivo studies, because the major commercial platform for global mRNA expression profiling does not reliably reflect RUNX1 levels. Our in vitro results indicate that hyperproliferation in RUNX1-deficient breast epithelia relies on another family of transcription factors, the Forkhead box O (FOXO) proteins. FOXOs could, therefore, represent a synthetic-lethal target for RUNX1-deficient tumors if the hypothesized link to breast cancer is correct.The transcription factor Runt-related transcription factor 1 (RUNX1) is critical for the earliest steps of hematopoiesis. RUNX1 was originally identified as a gene fusion in acute myeloid leukemia (AML) and thus has garnered heavy attention as a tumor suppressor in hematopoietic malignancies. However, RUNX1 is also strongly expressed in breast epithelia and may be misregulated during tumorigenesis. Here, I discuss our recent work implicating RUNX1 in proliferation control during breast epithelial-acinar morphogenesis. My goal is to place these findings in the context of a handful of other reports, which together argue that RUNX1 could act as a tumor suppressor gene in breast cancer. Testing this hypothesis requires focused in vivo studies, because the major commercial platform for global mRNA expression profiling does not reliably reflect RUNX1 levels. Our in vitro results indicate that hyperproliferation in RUNX1-deficient breast epithelia relies on another family of transcription factors, the Forkhead box O (FOXO) proteins. FOXOs could, therefore, represent a synthetic-lethal target for RUNX1-deficient tumors if the hypothesized link to breast cancer is correct. |
| Author | Janes, Kevin A. |
| AuthorAffiliation | 1Department of Biomedical Engineering; University of Virginia; Charlottesville, VA USA |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22024923$$D View this record in MEDLINE/PubMed |
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| Snippet | The transcription factor Runt-related transcription factor 1 (RUNX1) is critical for the earliest steps of hematopoiesis. RUNX1 was originally identified as a... |
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| SubjectTerms | Acinar Cells - metabolism Binding Biology Bioscience Breast Neoplasms - metabolism Cadherins - metabolism Calcium Cancer Cell Cell Proliferation Core Binding Factor Alpha 2 Subunit - deficiency Core Binding Factor Alpha 2 Subunit - genetics Core Binding Factor Alpha 2 Subunit - metabolism Cycle Extra View Female Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Gene Expression Profiling - methods Gene Knockdown Techniques Genes, Tumor Suppressor Humans Immunohistochemistry Landes Oligonucleotide Array Sequence Analysis - methods Organogenesis Proteins Tumor Cells, Cultured |
| Title | RUNX1 and its understudied role in breast cancer |
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