PPM1D Knockdown Suppresses Cell Proliferation, Promotes Cell Apoptosis, and Activates p38 MAPK/p53 Signaling Pathway in Acute Myeloid Leukemia
Objectives: This study was to explore the effect of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D knockdown on proliferation and apoptosis as well as p38 MAPK/p53 signaling pathway in acute myeloid leukemia. Methods: The expression of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D was detected in a...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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SAGE Publishing
2020-07-01
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| Series: | Technology in Cancer Research & Treatment |
| Online Access: | https://doi.org/10.1177/1533033820942312 |
| _version_ | 1818550782465671168 |
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| author | Bin Li MD Jie Hu MD Di He BS Qi Chen MD Suna Liu BS Xiaoling Zhu MD Meijia Yu MD |
| author_facet | Bin Li MD Jie Hu MD Di He BS Qi Chen MD Suna Liu BS Xiaoling Zhu MD Meijia Yu MD |
| author_sort | Bin Li MD |
| collection | DOAJ |
| description | Objectives: This study was to explore the effect of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D knockdown on proliferation and apoptosis as well as p38 MAPK/p53 signaling pathway in acute myeloid leukemia. Methods: The expression of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D was detected in acute myeloid leukemia cell lines including SKM-1, KG-1, AML-193, and THP-1 cells, and normal bone marrow mononuclear cells isolated from healthy donors. The knockdown of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D was conducted by transfecting small interfering RNA into AML-193 cells and KG-1 cells. Results: The relative messenger RNA/protein expressions of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D were higher in SKM-1, KG-1, AML-193, and THP-1 cells compared with control cells (normal bone marrow mononuclear cells). After transfecting protein phosphatase, Mg 2+ /Mn 2+ dependent 1D small interfering RNA into AML-193 cells and KG-1 cells, both messenger RNA and protein expressions of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D were significantly reduced, indicating the successful transfection. Most importantly, knockdown of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D suppressed cell proliferation and promoted cell apoptosis in AML-193 cells and KG-1 cells. In addition, knockdown of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D enhanced the expressions of p-p38 and p53 in AML-193 cells and KG-1 cells. The above observation suggested that protein phosphatase, Mg 2+ /Mn 2+ dependent 1D knockdown suppressed cell proliferation, promoted cell apoptosis, and activated p38 MAPK/p53 signaling pathway in acute myeloid leukemia cells. Conclusion: Protein phosphatase, Mg 2+ /Mn 2+ dependent 1D is implicated in acute myeloid leukemia carcinogenesis, which illuminates its potential role as a treatment target for acute myeloid leukemia. |
| first_indexed | 2024-12-12T08:51:06Z |
| format | Article |
| id | doaj.art-49ed602662d6488baa8c390ce185dd32 |
| institution | Directory Open Access Journal |
| issn | 1533-0338 |
| language | English |
| last_indexed | 2024-12-12T08:51:06Z |
| publishDate | 2020-07-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Technology in Cancer Research & Treatment |
| spelling | doaj.art-49ed602662d6488baa8c390ce185dd322022-12-22T00:30:14ZengSAGE PublishingTechnology in Cancer Research & Treatment1533-03382020-07-011910.1177/1533033820942312PPM1D Knockdown Suppresses Cell Proliferation, Promotes Cell Apoptosis, and Activates p38 MAPK/p53 Signaling Pathway in Acute Myeloid LeukemiaBin Li MD0Jie Hu MD1Di He BS2Qi Chen MD3Suna Liu BS4Xiaoling Zhu MD5Meijia Yu MD6 Department of Hematology, The Second People’s Hospital of Yunnan Province, Yunnan, China Department of Hematology, The Second People’s Hospital of Yunnan Province, Yunnan, China Department of Hematology, The Second People’s Hospital of Yunnan Province, Yunnan, China Department of Hematology, The Second People’s Hospital of Yunnan Province, Yunnan, China Department of Hematology, The Second People’s Hospital of Yunnan Province, Yunnan, China Department of Hematology, The Second People’s Hospital of Yunnan Province, Yunnan, China Department of Hematology, The Second People’s Hospital of Yunnan Province, Yunnan, ChinaObjectives: This study was to explore the effect of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D knockdown on proliferation and apoptosis as well as p38 MAPK/p53 signaling pathway in acute myeloid leukemia. Methods: The expression of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D was detected in acute myeloid leukemia cell lines including SKM-1, KG-1, AML-193, and THP-1 cells, and normal bone marrow mononuclear cells isolated from healthy donors. The knockdown of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D was conducted by transfecting small interfering RNA into AML-193 cells and KG-1 cells. Results: The relative messenger RNA/protein expressions of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D were higher in SKM-1, KG-1, AML-193, and THP-1 cells compared with control cells (normal bone marrow mononuclear cells). After transfecting protein phosphatase, Mg 2+ /Mn 2+ dependent 1D small interfering RNA into AML-193 cells and KG-1 cells, both messenger RNA and protein expressions of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D were significantly reduced, indicating the successful transfection. Most importantly, knockdown of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D suppressed cell proliferation and promoted cell apoptosis in AML-193 cells and KG-1 cells. In addition, knockdown of protein phosphatase, Mg 2+ /Mn 2+ dependent 1D enhanced the expressions of p-p38 and p53 in AML-193 cells and KG-1 cells. The above observation suggested that protein phosphatase, Mg 2+ /Mn 2+ dependent 1D knockdown suppressed cell proliferation, promoted cell apoptosis, and activated p38 MAPK/p53 signaling pathway in acute myeloid leukemia cells. Conclusion: Protein phosphatase, Mg 2+ /Mn 2+ dependent 1D is implicated in acute myeloid leukemia carcinogenesis, which illuminates its potential role as a treatment target for acute myeloid leukemia.https://doi.org/10.1177/1533033820942312 |
| spellingShingle | Bin Li MD Jie Hu MD Di He BS Qi Chen MD Suna Liu BS Xiaoling Zhu MD Meijia Yu MD PPM1D Knockdown Suppresses Cell Proliferation, Promotes Cell Apoptosis, and Activates p38 MAPK/p53 Signaling Pathway in Acute Myeloid Leukemia Technology in Cancer Research & Treatment |
| title | PPM1D Knockdown Suppresses Cell Proliferation, Promotes Cell Apoptosis, and Activates p38 MAPK/p53 Signaling Pathway in Acute Myeloid Leukemia |
| title_full | PPM1D Knockdown Suppresses Cell Proliferation, Promotes Cell Apoptosis, and Activates p38 MAPK/p53 Signaling Pathway in Acute Myeloid Leukemia |
| title_fullStr | PPM1D Knockdown Suppresses Cell Proliferation, Promotes Cell Apoptosis, and Activates p38 MAPK/p53 Signaling Pathway in Acute Myeloid Leukemia |
| title_full_unstemmed | PPM1D Knockdown Suppresses Cell Proliferation, Promotes Cell Apoptosis, and Activates p38 MAPK/p53 Signaling Pathway in Acute Myeloid Leukemia |
| title_short | PPM1D Knockdown Suppresses Cell Proliferation, Promotes Cell Apoptosis, and Activates p38 MAPK/p53 Signaling Pathway in Acute Myeloid Leukemia |
| title_sort | ppm1d knockdown suppresses cell proliferation promotes cell apoptosis and activates p38 mapk p53 signaling pathway in acute myeloid leukemia |
| url | https://doi.org/10.1177/1533033820942312 |
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