RapamycinFungusV1, Main, Exploration, bibRecord, 000431

Upregulation of AMPK by 4-O-methylascochlorin promotes autophagy via the HIF-1α expression.

Identifieur interne : 000431 ( Main/Exploration ); précédent : 000430; suivant : 000432

Upregulation of AMPK by 4-O-methylascochlorin promotes autophagy via the HIF-1α expression.

Auteurs : Ji-Young Seok [Corée du Sud] ; Yun-Jeong Jeong [Corée du Sud] ; Soon-Kyung Hwang [Corée du Sud] ; Cheorl-Ho Kim [Corée du Sud] ; Junji Magae [Japon] ; Young-Chae Chang [Corée du Sud]

Source :

Journal of cellular and molecular medicine [ 1582-4934 ] ; 2018.

RBID : pubmed:30338933

Descripteurs français

English descriptors

KwdEn :
- Anti-Bacterial Agents (chemistry), Anti-Bacterial Agents (pharmacology), Apoptosis (drug effects), Ascomycota (chemistry), Autophagy (drug effects), Cell Hypoxia (drug effects), Cell Line, Tumor (MeSH), Cell Survival (drug effects), Gene Expression Regulation, Neoplastic (drug effects), Humans (MeSH), Hypoxia-Inducible Factor 1, alpha Subunit (genetics), Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (pathology), Membrane Proteins (genetics), Microtubule-Associated Proteins (genetics), Phosphorylation (drug effects), Proto-Oncogene Proteins (genetics), Signal Transduction (drug effects), TOR Serine-Threonine Kinases (genetics), Terpenes (chemistry), Terpenes (pharmacology), Transcriptional Activation (drug effects).
MESH :
- chemical , chemistry : Anti-Bacterial Agents, Terpenes.
- chemical , genetics : Hypoxia-Inducible Factor 1, alpha Subunit, Membrane Proteins, Microtubule-Associated Proteins, Proto-Oncogene Proteins, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Anti-Bacterial Agents, Terpenes.
- chemistry : Ascomycota.
- drug effects : Apoptosis, Autophagy, Cell Hypoxia, Cell Survival, Gene Expression Regulation, Neoplastic, Phosphorylation, Signal Transduction, Transcriptional Activation.
- drug therapy : Lung Neoplasms.
- genetics : Lung Neoplasms.
- pathology : Lung Neoplasms.
- Cell Line, Tumor, Humans.

Abstract

4-O-methylascochlorin (MAC) is a derivative of ascochlorin, a prenyl-phenol compound antibiotic isolated from the fungus Ascochyta viciae. MAC induces caspase/poly (ADP-ribose) polymerase-mediated apoptosis in leukemia cells. However, the effects of MAC on autophagy in cancer cells and the underlying molecular mechanisms remain unknown. Here, we show that MAC induces autophagy in lung cancer cells. MAC significantly induced the expression of autophagy marker proteins including LC3-II, Beclin1, and ATG7. MAC promoted AMP-activated protein kinase (AMPK) phosphorylation and inhibited the phosphorylation of mammalian target of rapamycin (mTOR) and its downstream signalling proteins P70S6K and 4EBP1. The AMPK activator AICAR upregulated LC3-II expression through the AMPK/mTOR pathway similar to the effects of MAC. MAC-induced LC3-II protein expression was slightly reduced in AMPK siRNA transfected cells. MAC upregulated hypoxia-inducible factor-1α (HIF-1α) and BNIP3, which are HIF-1α-dependent autophagic proteins. Treatment with CoCl₂ , which mimics hypoxia, induced autophagy similar to the effect of MAC. The HIF-1α inhibitor YC-1 and HIF-1α siRNA inhibited the MAC-induced upregulation of LC3-II and BNIP3. These results suggest that MAC induces autophagy via the AMPK/mTOR signalling pathway and by upregulating HIF-1α and BNIP3 protein expression in lung cancer cells.

DOI: 10.1111/jcmm.13933
PubMed: 30338933
PubMed Central: PMC6237564

Affiliations:

Corée du Sud, Japon

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000427
to stream Main, to step Curation: 000427

Le document en format XML

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<term>Ascomycota (chemistry)</term>
<term>Autophagy (drug effects)</term>
<term>Cell Hypoxia (drug effects)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Survival (drug effects)</term>
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<term>Protéines associées aux microtubules (génétique)</term>
<term>Protéines membranaires (génétique)</term>
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<front><div type="abstract" xml:lang="en">4-O-methylascochlorin (MAC) is a derivative of ascochlorin, a prenyl-phenol compound antibiotic isolated from the fungus Ascochyta viciae. MAC induces caspase/poly (ADP-ribose) polymerase-mediated apoptosis in leukemia cells. However, the effects of MAC on autophagy in cancer cells and the underlying molecular mechanisms remain unknown. Here, we show that MAC induces autophagy in lung cancer cells. MAC significantly induced the expression of autophagy marker proteins including LC3-II, Beclin1, and ATG7. MAC promoted AMP-activated protein kinase (AMPK) phosphorylation and inhibited the phosphorylation of mammalian target of rapamycin (mTOR) and its downstream signalling proteins P70S6K and 4EBP1. The AMPK activator AICAR upregulated LC3-II expression through the AMPK/mTOR pathway similar to the effects of MAC. MAC-induced LC3-II protein expression was slightly reduced in AMPK siRNA transfected cells. MAC upregulated hypoxia-inducible factor-1α (HIF-1α) and BNIP3, which are HIF-1α-dependent autophagic proteins. Treatment with CoCl<sub>2</sub>
 , which mimics hypoxia, induced autophagy similar to the effect of MAC. The HIF-1α inhibitor YC-1 and HIF-1α siRNA inhibited the MAC-induced upregulation of LC3-II and BNIP3. These results suggest that MAC induces autophagy via the AMPK/mTOR signalling pathway and by upregulating HIF-1α and BNIP3 protein expression in lung cancer cells.</div>
</front>
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<Abstract><AbstractText>4-O-methylascochlorin (MAC) is a derivative of ascochlorin, a prenyl-phenol compound antibiotic isolated from the fungus Ascochyta viciae. MAC induces caspase/poly (ADP-ribose) polymerase-mediated apoptosis in leukemia cells. However, the effects of MAC on autophagy in cancer cells and the underlying molecular mechanisms remain unknown. Here, we show that MAC induces autophagy in lung cancer cells. MAC significantly induced the expression of autophagy marker proteins including LC3-II, Beclin1, and ATG7. MAC promoted AMP-activated protein kinase (AMPK) phosphorylation and inhibited the phosphorylation of mammalian target of rapamycin (mTOR) and its downstream signalling proteins P70S6K and 4EBP1. The AMPK activator AICAR upregulated LC3-II expression through the AMPK/mTOR pathway similar to the effects of MAC. MAC-induced LC3-II protein expression was slightly reduced in AMPK siRNA transfected cells. MAC upregulated hypoxia-inducible factor-1α (HIF-1α) and BNIP3, which are HIF-1α-dependent autophagic proteins. Treatment with CoCl<sub>2</sub>
 , which mimics hypoxia, induced autophagy similar to the effect of MAC. The HIF-1α inhibitor YC-1 and HIF-1α siRNA inhibited the MAC-induced upregulation of LC3-II and BNIP3. These results suggest that MAC induces autophagy via the AMPK/mTOR signalling pathway and by upregulating HIF-1α and BNIP3 protein expression in lung cancer cells.</AbstractText>
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	Serveur d'exploration sur la rapamycine et les champignons
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Upregulation of AMPK by 4-O-methylascochlorin promotes autophagy via the HIF-1α expression.

Upregulation of AMPK by 4-O-methylascochlorin promotes autophagy via the HIF-1α expression.

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