ArticleExperimental and therapeutic medicine2018
Prolyl oligopeptidase inhibitor suppresses the upregulation of ACSDKP in patients with acute myeloid leukemia.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 2 citations in OpenAlex.
- Computer-Aided Drug Discovery Identifies Alkaloid Inhibitors of Parkinson's Disease Associated Protein, Prolyl Oligopeptidase.Evidence-based complementary and alternative medicine : eCAM · 2021Article
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4 authors at 2 institutions in 1 country.
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Abstract
The aim of the current study was to measure the expression of acetyl-N-Ser-Asp-Lys-Pro (ACSDKP) in patients with acute myeloid leukemia (AML) and the effect of prolyl oligopeptidase inhibitor (POPi) on the bone marrow stromal cells of these patients. Serum and bone marrow stromal cell samples were collected from 33 patients with AML admitted to Wuxi Second People's Hospital, Nanjing Medical University between September 2011 and August 2016. ACSDKP levels were measured using a highly specific competitive enzyme immunoassay (EIA). Bone marrow stromal cells were treated with synthetic ACSDKP (10 µM/ml) or different concentrations of POPi S17092 (25, 50 and 100 µg/ml). Cells that received no treatment were used as control. An MTT assay was conducted to measure the proliferation of bone marrow stromal cells. The results demonstrated that serum levels of ACSDKP in patients with AML were significantly higher than those of controls (P<0.05). Following treatment with ACSDKP, cell proliferation was significantly increased compared with untreated cells (P<0.05). However, following treatment with different concentrations of POPi, the expression of ACSDKP was significantly decreased in a dose-dependent manner (P<0.05). Furthermore, the proliferation of bone marrow stromal cells was also decreased in a dose-dependent manner. Therefore, the present study demonstrated that ACSDKP levels were increased in the serum and bone marrow stromal cells of patients with AML and that ACSDKP promoted the proliferation of bone marrow stromal cells of these patients, which was inhibited by POPi. These results may identify a novel target for the treatment of AML.
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