Alpha-enolase promotes progression of acute myeloid leukemia via MAPK/ERK signaling pathway
Due to the limited availability of effective treatment therapies, patients with refractory and relapsed acute myeloid leukemia (AML) often have poor prognoses. Therefore, identifying new therapeutic targets to improve the treatment landscape and enhance AML outcomes is critical. In this study, we de...
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Health
2025-09-01
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| Series: | Blood Science |
| Online Access: | http://journals.lww.com/10.1097/BS9.0000000000000246 |
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| _version_ | 1849222757279072256 |
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| author | Shanshan Zhang Haina Wang Xuehong Zhang Xiangjie Kui Dan Huang Menglu Qin Shuqing Liu Ming-Zhong Sun Jinsong Yan |
| author_facet | Shanshan Zhang Haina Wang Xuehong Zhang Xiangjie Kui Dan Huang Menglu Qin Shuqing Liu Ming-Zhong Sun Jinsong Yan |
| author_sort | Shanshan Zhang |
| collection | DOAJ |
| description | Due to the limited availability of effective treatment therapies, patients with refractory and relapsed acute myeloid leukemia (AML) often have poor prognoses. Therefore, identifying new therapeutic targets to improve the treatment landscape and enhance AML outcomes is critical. In this study, we demonstrated for the first time that alpha-enolase (ENO1) is markedly overexpressed in AML and is closely associated with poor prognosis. In vitro experiments revealed that ENO1 knockdown (shENO1) significantly inhibited cell proliferation and invasion, and concomitantly induced cell cycle arrest. In vivo, a mouse model engrafted with U937-shENO1 cells exhibited markedly prolonged overall survival compared with a model implanted with U937 cells. Mechanistically, ENO1 operates by activating the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway, as evidenced by the reversal of shENO1 function through ERK activation. Collectively, our findings highlight ENO1 as a promising therapeutic target in AML. |
| format | Article |
| id | doaj-art-b2f3944a97114251832b010c623ecfbd |
| institution | Kabale University |
| issn | 2543-6368 |
| language | English |
| publishDate | 2025-09-01 |
| publisher | Wolters Kluwer Health |
| record_format | Article |
| series | Blood Science |
| spelling | doaj-art-b2f3944a97114251832b010c623ecfbd2025-08-26T03:22:27ZengWolters Kluwer HealthBlood Science2543-63682025-09-0173e0024610.1097/BS9.0000000000000246202509000-00008Alpha-enolase promotes progression of acute myeloid leukemia via MAPK/ERK signaling pathwayShanshan Zhang0Haina Wang1Xuehong Zhang2Xiangjie Kui3Dan Huang4Menglu Qin5Shuqing Liu6Ming-Zhong Sun7Jinsong Yan8a Department of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, Chinaa Department of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, Chinad Center of Genome and Personalized Medicine, Institute of Cancer Stem Cell, Dalian Medical University, Dalian 116044, Chinaa Department of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, Chinaa Department of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, Chinac Liaoning Key Laboratory of Hematopoietic Stem Cell Transplantation and Translational Medicine, Blood Stem Cell Transplantation Institute, Dalian Key Laboratory of hematology, Diamond Bay Institute of Hematology, the Second Hospital of Dalian Medical University, Dalian 116027, Chinae Department of Biochemistry, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, Chinab Department of Biotechnology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, Chinaa Department of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, ChinaDue to the limited availability of effective treatment therapies, patients with refractory and relapsed acute myeloid leukemia (AML) often have poor prognoses. Therefore, identifying new therapeutic targets to improve the treatment landscape and enhance AML outcomes is critical. In this study, we demonstrated for the first time that alpha-enolase (ENO1) is markedly overexpressed in AML and is closely associated with poor prognosis. In vitro experiments revealed that ENO1 knockdown (shENO1) significantly inhibited cell proliferation and invasion, and concomitantly induced cell cycle arrest. In vivo, a mouse model engrafted with U937-shENO1 cells exhibited markedly prolonged overall survival compared with a model implanted with U937 cells. Mechanistically, ENO1 operates by activating the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway, as evidenced by the reversal of shENO1 function through ERK activation. Collectively, our findings highlight ENO1 as a promising therapeutic target in AML.http://journals.lww.com/10.1097/BS9.0000000000000246 |
| spellingShingle | Shanshan Zhang Haina Wang Xuehong Zhang Xiangjie Kui Dan Huang Menglu Qin Shuqing Liu Ming-Zhong Sun Jinsong Yan Alpha-enolase promotes progression of acute myeloid leukemia via MAPK/ERK signaling pathway Blood Science |
| title | Alpha-enolase promotes progression of acute myeloid leukemia via MAPK/ERK signaling pathway |
| title_full | Alpha-enolase promotes progression of acute myeloid leukemia via MAPK/ERK signaling pathway |
| title_fullStr | Alpha-enolase promotes progression of acute myeloid leukemia via MAPK/ERK signaling pathway |
| title_full_unstemmed | Alpha-enolase promotes progression of acute myeloid leukemia via MAPK/ERK signaling pathway |
| title_short | Alpha-enolase promotes progression of acute myeloid leukemia via MAPK/ERK signaling pathway |
| title_sort | alpha enolase promotes progression of acute myeloid leukemia via mapk erk signaling pathway |
| url | http://journals.lww.com/10.1097/BS9.0000000000000246 |
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