Effects of a spiroketal compound Peniciketal A and its molecular mechanisms on growth inhibition in human leukemia.
Identifieur interne : 000368 ( Main/Corpus ); précédent : 000367; suivant : 000369Effects of a spiroketal compound Peniciketal A and its molecular mechanisms on growth inhibition in human leukemia.
Auteurs : Xue Gao ; Yuming Zhou ; Hongliu Sun ; Desheng Liu ; Jing Zhang ; Junru Zhang ; Weizhong Liu ; Xiaohong PanSource :
- Toxicology and applied pharmacology [ 1096-0333 ] ; 2019.
English descriptors
- KwdEn :
- AMP-Activated Protein Kinases (metabolism), Animals (MeSH), Antineoplastic Agents (pharmacology), Antineoplastic Agents (toxicity), Apoptosis (drug effects), Apoptosis Regulatory Proteins (metabolism), Autophagy (drug effects), Autophagy-Related Proteins (metabolism), Cell Cycle Checkpoints (drug effects), Cell Proliferation (MeSH), Chromatography, High Pressure Liquid (MeSH), HL-60 Cells (MeSH), Humans (MeSH), K562 Cells (MeSH), Leukemia (drug therapy), Leukemia (metabolism), Leukemia (pathology), Mice (MeSH), Proteomics (methods), Pyrans (pharmacology), Pyrans (toxicity), Signal Transduction (drug effects), Spiro Compounds (pharmacology), Spiro Compounds (toxicity), THP-1 Cells (MeSH), TOR Serine-Threonine Kinases (metabolism), Tandem Mass Spectrometry (MeSH).
- MESH :
- chemical , metabolism : AMP-Activated Protein Kinases, Apoptosis Regulatory Proteins, Autophagy-Related Proteins, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Antineoplastic Agents, Pyrans, Spiro Compounds.
- chemical , toxicity : Antineoplastic Agents, Pyrans, Spiro Compounds.
- drug effects : Apoptosis, Autophagy, Cell Cycle Checkpoints, Signal Transduction.
- drug therapy : Leukemia.
- metabolism : Leukemia.
- methods : Proteomics.
- pathology : Leukemia.
- Animals, Cell Proliferation, Chromatography, High Pressure Liquid, HL-60 Cells, Humans, K562 Cells, Mice, THP-1 Cells, Tandem Mass Spectrometry.
Abstract
Peniciketal A (Pe-A), a spiroketal compound, is isolated from the saline soil-derived fungus Penicillium raistrickii. However, the underlying molecular mechanistic basis for the effects of Pe-A on leukemia is poorly understood. Here, we investigated that Pe-A reduced cell proliferation in three leukemia cell lines (THP-1, K562 and HL60). Importantly, Pe-A showed little cytotoxicity in primary mouse embryonic fibroblast (MEF) cells in a long-duration treatment. For the mechanistic research, we identified 3449 differentially expressed Pe-A-induced proteins through liquid chromatography-tandem mass spectrometry (LC-MS/MS) with TMT label in THP-1 cells. Results showed that many identified proteins were involved in apoptosis and/or autophagy. Then, we confirmed that Pe-A induced not only apoptosis via the mitochondrial pathway but also cytoprotective autophagy by activating the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway indeed. In addition, Pe-A also arrested the cell cycle at the G0-G1 phase by regulating the expressions of checkpoint protein. Collectively, these results provide new insights into the mechanisms that Pe-A may target autophagy-related or apoptosis-related pathways to suppress the development of human leukemia.
DOI: 10.1016/j.taap.2018.12.007
PubMed: 30660475
Links to Exploration step
pubmed:30660475Le document en format XML
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<term>Antineoplastic Agents (toxicity)</term>
<term>Apoptosis (drug effects)</term>
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<term>Autophagy (drug effects)</term>
<term>Autophagy-Related Proteins (metabolism)</term>
<term>Cell Cycle Checkpoints (drug effects)</term>
<term>Cell Proliferation (MeSH)</term>
<term>Chromatography, High Pressure Liquid (MeSH)</term>
<term>HL-60 Cells (MeSH)</term>
<term>Humans (MeSH)</term>
<term>K562 Cells (MeSH)</term>
<term>Leukemia (drug therapy)</term>
<term>Leukemia (metabolism)</term>
<term>Leukemia (pathology)</term>
<term>Mice (MeSH)</term>
<term>Proteomics (methods)</term>
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<term>Signal Transduction (drug effects)</term>
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<term>Spiro Compounds (toxicity)</term>
<term>THP-1 Cells (MeSH)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Tandem Mass Spectrometry (MeSH)</term>
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<term>Autophagy-Related Proteins</term>
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<term>HL-60 Cells</term>
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<front><div type="abstract" xml:lang="en">Peniciketal A (Pe-A), a spiroketal compound, is isolated from the saline soil-derived fungus Penicillium raistrickii. However, the underlying molecular mechanistic basis for the effects of Pe-A on leukemia is poorly understood. Here, we investigated that Pe-A reduced cell proliferation in three leukemia cell lines (THP-1, K562 and HL60). Importantly, Pe-A showed little cytotoxicity in primary mouse embryonic fibroblast (MEF) cells in a long-duration treatment. For the mechanistic research, we identified 3449 differentially expressed Pe-A-induced proteins through liquid chromatography-tandem mass spectrometry (LC-MS/MS) with TMT label in THP-1 cells. Results showed that many identified proteins were involved in apoptosis and/or autophagy. Then, we confirmed that Pe-A induced not only apoptosis via the mitochondrial pathway but also cytoprotective autophagy by activating the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway indeed. In addition, Pe-A also arrested the cell cycle at the G0-G1 phase by regulating the expressions of checkpoint protein. Collectively, these results provide new insights into the mechanisms that Pe-A may target autophagy-related or apoptosis-related pathways to suppress the development of human leukemia.</div>
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<Abstract><AbstractText>Peniciketal A (Pe-A), a spiroketal compound, is isolated from the saline soil-derived fungus Penicillium raistrickii. However, the underlying molecular mechanistic basis for the effects of Pe-A on leukemia is poorly understood. Here, we investigated that Pe-A reduced cell proliferation in three leukemia cell lines (THP-1, K562 and HL60). Importantly, Pe-A showed little cytotoxicity in primary mouse embryonic fibroblast (MEF) cells in a long-duration treatment. For the mechanistic research, we identified 3449 differentially expressed Pe-A-induced proteins through liquid chromatography-tandem mass spectrometry (LC-MS/MS) with TMT label in THP-1 cells. Results showed that many identified proteins were involved in apoptosis and/or autophagy. Then, we confirmed that Pe-A induced not only apoptosis via the mitochondrial pathway but also cytoprotective autophagy by activating the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway indeed. In addition, Pe-A also arrested the cell cycle at the G0-G1 phase by regulating the expressions of checkpoint protein. Collectively, these results provide new insights into the mechanisms that Pe-A may target autophagy-related or apoptosis-related pathways to suppress the development of human leukemia.</AbstractText>
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