ArticleCancer medicine2019
LukS-PV induces apoptosis in acute myeloid leukemia cells mediated by C5a receptor.
Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Toxin protein LukS-PV targeting complement receptor C5aR1 inhibits cell proliferation in hepatocellular carcinoma via the HDAC7-Wnt/β-catenin axis.The Journal of biological chemistry · 2025Article
- Exploration of compounds to inhibit the Panton-Valentine leukocidin of Staphylococcus aureus.Medical microbiology and immunology · 2024Article
- The anticancer effect of recombinant LukS-PV protein and silver nanoparticles loaded with this protein.AMB Express · 2023Article
- Methicillin-ResistantPathogens (Basel, Switzerland) · 2022Article
- LukS-PV Induces ApoptosisFrontiers in oncology · 2021Article
- LukS-PV Inhibits Hepatocellular Carcinoma Progression by Downregulating HDAC2 Expression.Molecular therapy oncolytics · 2020Article
- Quantitative proteomic analysis reveals that Luks-PV exerts antitumor activity by regulating the key proteins and metabolic pathways in HepG2 cells.Anti-cancer drugs · 2020Article
- LukS-PV Inhibits Hepatocellular Carcinoma Cells Migration via the TNNC1/PI3K/AKT Axis.OncoTargets and therapy · 2020Article
- Article
- LukS-PV induces apoptosis in acute myeloid leukemia cells mediated by C5a receptor.Cancer medicine · 2019Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LukS-PV is one of the two components of Panton-Valentine leucocidin (PVL). Our previous study showed that LukS-PV can induce apoptosis in human acute myeloid leukemia (AML) THP-1 and HL-60 cells. C5aR (C5a receptor) is the receptor for PVL, but whether C5aR plays a key role in LukS-PV induced apoptosis is unclear. The aim of this study was to establish whether C5aR plays a physiological role in apoptosis of leukemia cells induced by LukS-PV. We investigated the role of C5aR in leukemia cell apoptosis induced by LukS-PV by pretreatment of THP-1 and HL-60 cells with C5aR antagonist and transfection to knockdown C5aR in THP-1 cells or overexpress C5aR in Jurkat cells before treatment with LukS-PV. Cell apoptosis was analyzed by staining with Annexin V/propidium iodide or Annexin V-PE/7-AAD. Mitochondrial membrane potential (MMP) was determined using JC-1 dye. The expression of apoptosis-associated genes and proteins was identified by qRT-polymerase chain reaction and Western blotting analysis, respectively. As the C5aR antagonist concentration increased, the rate of apoptosis induced by LukS-PV decreased, the MMP increased, and expression of pro-apoptotic Bax and Bak genes and proteins was downregulated while that of anti-apoptotic Bcl-2 and Bcl-x genes and proteins was upregulated. Knockdown of C5aR also decreased LukS-PV-induced THP-1 cell apoptosis. LukS-PV did not induce apoptosis of Jurkat cells, which have no endogenous C5aR expression; however, LukS-PV did induce apoptosis in Jurkat cells after overexpression of C5aR. Correspondingly, the MMP decreased and Bax and Bak were upregulated while Bcl-2 and Bcl-x were downregulated. LukS-PV can induce apoptosis in AML cells by targeting C5aR. C5aR may be a potential therapeutic target for AML and LukS-PV is a candidate targeted drug for the treatment of AML.
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