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A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia
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| Zeitschriftentitel: | Blood |
|---|---|
| Personen und Körperschaften: | , , , , , , |
| In: | Blood, 118, 2011, 2, S. 390-400 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Society of Hematology
|
| Schlagwörter: |
| author_facet |
Chen, Yaoyu Sullivan, Con Peng, Cong Shan, Yi Hu, Yiguo Li, Dongguang Li, Shaoguang Chen, Yaoyu Sullivan, Con Peng, Cong Shan, Yi Hu, Yiguo Li, Dongguang Li, Shaoguang |
|---|---|
| author |
Chen, Yaoyu Sullivan, Con Peng, Cong Shan, Yi Hu, Yiguo Li, Dongguang Li, Shaoguang |
| spellingShingle |
Chen, Yaoyu Sullivan, Con Peng, Cong Shan, Yi Hu, Yiguo Li, Dongguang Li, Shaoguang Blood A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia Cell Biology Hematology Immunology Biochemistry |
| author_sort |
chen, yaoyu |
| spelling |
Chen, Yaoyu Sullivan, Con Peng, Cong Shan, Yi Hu, Yiguo Li, Dongguang Li, Shaoguang 0006-4971 1528-0020 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood-2010-11-316760 <jats:title>Abstract</jats:title> <jats:p>We have shown that Alox5 is a critical regulator of leukemia stem cells (LSCs) in a BCR-ABL–induced chronic myeloid leukemia (CML) mouse model, and we hypothesize that the Alox5 pathway represents a major molecular network that regulates LSC function. Therefore, we sought to dissect this pathway by comparing the gene expression profiles of wild type and Alox5−/− LSCs. DNA microarray analysis revealed a small group of candidate genes that exhibited changes in the levels of transcription in the absence of Alox5 expression. In particular, we noted that the expression of the Msr1 gene was upregulated in Alox5−/− LSCs, suggesting that Msr1 suppresses the proliferation of LSCs. Using CML mouse model, we show that Msr1 is downregulated by BCR-ABL and this down-regulation is partially restored by Alox5 deletion, and that Msr1 deletion causes acceleration of CML development. Moreover, Msr1 deletion markedly increases LSC function through its effects on cell cycle progression and apoptosis. We also show that Msr1 affects CML development by regulating the PI3K-AKT pathway and β-Catenin. Together, these results demonstrate that Msr1 suppresses LSCs and CML development. The enhancement of the tumor suppressor function of Msr1 may be of significance in the development of novel therapeutic strategies for CML.</jats:p> A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia Blood |
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10.1182/blood-2010-11-316760 |
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| title |
A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_unstemmed |
A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_full |
A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_fullStr |
A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_full_unstemmed |
A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_short |
A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_sort |
a tumor suppressor function of the msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| topic |
Cell Biology Hematology Immunology Biochemistry |
| url |
http://dx.doi.org/10.1182/blood-2010-11-316760 |
| publishDate |
2011 |
| physical |
390-400 |
| description |
<jats:title>Abstract</jats:title>
<jats:p>We have shown that Alox5 is a critical regulator of leukemia stem cells (LSCs) in a BCR-ABL–induced chronic myeloid leukemia (CML) mouse model, and we hypothesize that the Alox5 pathway represents a major molecular network that regulates LSC function. Therefore, we sought to dissect this pathway by comparing the gene expression profiles of wild type and Alox5−/− LSCs. DNA microarray analysis revealed a small group of candidate genes that exhibited changes in the levels of transcription in the absence of Alox5 expression. In particular, we noted that the expression of the Msr1 gene was upregulated in Alox5−/− LSCs, suggesting that Msr1 suppresses the proliferation of LSCs. Using CML mouse model, we show that Msr1 is downregulated by BCR-ABL and this down-regulation is partially restored by Alox5 deletion, and that Msr1 deletion causes acceleration of CML development. Moreover, Msr1 deletion markedly increases LSC function through its effects on cell cycle progression and apoptosis. We also show that Msr1 affects CML development by regulating the PI3K-AKT pathway and β-Catenin. Together, these results demonstrate that Msr1 suppresses LSCs and CML development. The enhancement of the tumor suppressor function of Msr1 may be of significance in the development of novel therapeutic strategies for CML.</jats:p> |
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| author | Chen, Yaoyu, Sullivan, Con, Peng, Cong, Shan, Yi, Hu, Yiguo, Li, Dongguang, Li, Shaoguang |
| author_facet | Chen, Yaoyu, Sullivan, Con, Peng, Cong, Shan, Yi, Hu, Yiguo, Li, Dongguang, Li, Shaoguang, Chen, Yaoyu, Sullivan, Con, Peng, Cong, Shan, Yi, Hu, Yiguo, Li, Dongguang, Li, Shaoguang |
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| description | <jats:title>Abstract</jats:title> <jats:p>We have shown that Alox5 is a critical regulator of leukemia stem cells (LSCs) in a BCR-ABL–induced chronic myeloid leukemia (CML) mouse model, and we hypothesize that the Alox5 pathway represents a major molecular network that regulates LSC function. Therefore, we sought to dissect this pathway by comparing the gene expression profiles of wild type and Alox5−/− LSCs. DNA microarray analysis revealed a small group of candidate genes that exhibited changes in the levels of transcription in the absence of Alox5 expression. In particular, we noted that the expression of the Msr1 gene was upregulated in Alox5−/− LSCs, suggesting that Msr1 suppresses the proliferation of LSCs. Using CML mouse model, we show that Msr1 is downregulated by BCR-ABL and this down-regulation is partially restored by Alox5 deletion, and that Msr1 deletion causes acceleration of CML development. Moreover, Msr1 deletion markedly increases LSC function through its effects on cell cycle progression and apoptosis. We also show that Msr1 affects CML development by regulating the PI3K-AKT pathway and β-Catenin. Together, these results demonstrate that Msr1 suppresses LSCs and CML development. The enhancement of the tumor suppressor function of Msr1 may be of significance in the development of novel therapeutic strategies for CML.</jats:p> |
| doi_str_mv | 10.1182/blood-2010-11-316760 |
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| imprint_str_mv | American Society of Hematology, 2011 |
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| spelling | Chen, Yaoyu Sullivan, Con Peng, Cong Shan, Yi Hu, Yiguo Li, Dongguang Li, Shaoguang 0006-4971 1528-0020 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood-2010-11-316760 <jats:title>Abstract</jats:title> <jats:p>We have shown that Alox5 is a critical regulator of leukemia stem cells (LSCs) in a BCR-ABL–induced chronic myeloid leukemia (CML) mouse model, and we hypothesize that the Alox5 pathway represents a major molecular network that regulates LSC function. Therefore, we sought to dissect this pathway by comparing the gene expression profiles of wild type and Alox5−/− LSCs. DNA microarray analysis revealed a small group of candidate genes that exhibited changes in the levels of transcription in the absence of Alox5 expression. In particular, we noted that the expression of the Msr1 gene was upregulated in Alox5−/− LSCs, suggesting that Msr1 suppresses the proliferation of LSCs. Using CML mouse model, we show that Msr1 is downregulated by BCR-ABL and this down-regulation is partially restored by Alox5 deletion, and that Msr1 deletion causes acceleration of CML development. Moreover, Msr1 deletion markedly increases LSC function through its effects on cell cycle progression and apoptosis. We also show that Msr1 affects CML development by regulating the PI3K-AKT pathway and β-Catenin. Together, these results demonstrate that Msr1 suppresses LSCs and CML development. The enhancement of the tumor suppressor function of Msr1 may be of significance in the development of novel therapeutic strategies for CML.</jats:p> A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia Blood |
| spellingShingle | Chen, Yaoyu, Sullivan, Con, Peng, Cong, Shan, Yi, Hu, Yiguo, Li, Dongguang, Li, Shaoguang, Blood, A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia, Cell Biology, Hematology, Immunology, Biochemistry |
| title | A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_full | A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_fullStr | A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_full_unstemmed | A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_short | A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_sort | a tumor suppressor function of the msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| title_unstemmed | A tumor suppressor function of the Msr1 gene in leukemia stem cells of chronic myeloid leukemia |
| topic | Cell Biology, Hematology, Immunology, Biochemistry |
| url | http://dx.doi.org/10.1182/blood-2010-11-316760 |