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Modulation of autophagy in exJSRV-env-transfected cells through the Akt/mTOR and MAPK signaling pathway.

Identifieur interne : 000796 ( Main/Exploration ); précédent : 000795; suivant : 000797

Modulation of autophagy in exJSRV-env-transfected cells through the Akt/mTOR and MAPK signaling pathway.

Auteurs : Xiaolin Sun [République populaire de Chine] ; Fangyuan Du [République populaire de Chine] ; Shuying Liu [République populaire de Chine]

Source :

RBID : pubmed:28235485

Descripteurs français

English descriptors

Abstract

The envelope (Env) of Jaagsiekte sheep retrovirus (JSRV) is an oncoprotein of ovine pulmonary adenocarcinoma (OPA). Autophagy is involved in different cancers, but how it is carcinogenic in JSRV Env is unclear. Modulation of autophagy in exJSRV-env-NM-transfected cells through the Akt/mTOR and MAPK signaling pathway was studied, and we observed strong positive labeling of p-Akt, p-mTOR, p-MEK1/2, p-ERK1/2, p-p38 and p-JNK in tumor cells and typical type II pneumocytes in naturally infected OPA lung tissues, which was co-aligned with JSRV-Env positive cells as shown by immunohistochemical and microscopic analysis. Akt/mTOR and MAPK pathways were activated in OPA lung and JSRV-Env transfected NIH 3T3 cells. Decreased Beclin1 and LC3 II/I suggested that autophagy was inhibited in OPA lung and JSRV-Env transfected NIH 3T3 cells. Beclin1 and LC3 II/I increased in JSRV-Env transfected NIH3T3 cells treated with mTOR inhibitor (rapamycin), ERK1/2 inhibitor (PD 98059), p38 inhibitor (SB 203580) and JNK inhibitor (SP 600125), suggesting that Akt/mTOR and MAPK pathways were responsible for JSRV-Env decreased autophagy. In conclusion, JSRV Env decreased autophagy in JSRV-Env transfected NIH3T3 cells through Akt/mTOR and MAPK pathways, in particular, JNK and p38 pathways.

DOI: 10.1016/j.bbrc.2017.02.099
PubMed: 28235485


Affiliations:


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Le document en format XML

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<term>Fibroblasts (metabolism)</term>
<term>Fibroblasts (virology)</term>
<term>Gene Products, env (genetics)</term>
<term>Gene Products, env (metabolism)</term>
<term>Host-Pathogen Interactions (MeSH)</term>
<term>Immunoblotting (MeSH)</term>
<term>Immunohistochemistry (MeSH)</term>
<term>JNK Mitogen-Activated Protein Kinases (metabolism)</term>
<term>Jaagsiekte sheep retrovirus (genetics)</term>
<term>Jaagsiekte sheep retrovirus (metabolism)</term>
<term>Jaagsiekte sheep retrovirus (physiology)</term>
<term>Lung (metabolism)</term>
<term>Lung (virology)</term>
<term>MAP Kinase Signaling System (MeSH)</term>
<term>Mice (MeSH)</term>
<term>NIH 3T3 Cells (MeSH)</term>
<term>Phosphorylation (MeSH)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Pulmonary Adenomatosis, Ovine (genetics)</term>
<term>Pulmonary Adenomatosis, Ovine (metabolism)</term>
<term>Pulmonary Adenomatosis, Ovine (virology)</term>
<term>Sheep (MeSH)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>p38 Mitogen-Activated Protein Kinases (metabolism)</term>
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<term>Adénomatose pulmonaire ovine (génétique)</term>
<term>Adénomatose pulmonaire ovine (métabolisme)</term>
<term>Adénomatose pulmonaire ovine (virologie)</term>
<term>Animaux (MeSH)</term>
<term>Autophagie (MeSH)</term>
<term>Cellules NIH 3T3 (MeSH)</term>
<term>Extracellular Signal-Regulated MAP Kinases (métabolisme)</term>
<term>Fibroblastes (métabolisme)</term>
<term>Fibroblastes (virologie)</term>
<term>Immunohistochimie (MeSH)</term>
<term>Immunotransfert (MeSH)</term>
<term>Interactions hôte-pathogène (MeSH)</term>
<term>JNK Mitogen-Activated Protein Kinases (métabolisme)</term>
<term>Ovis (MeSH)</term>
<term>Phosphorylation (MeSH)</term>
<term>Poumon (métabolisme)</term>
<term>Poumon (virologie)</term>
<term>Produits du gène env (génétique)</term>
<term>Produits du gène env (métabolisme)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Rétrovirus Jaagsiekte du mouton (génétique)</term>
<term>Rétrovirus Jaagsiekte du mouton (métabolisme)</term>
<term>Rétrovirus Jaagsiekte du mouton (physiologie)</term>
<term>Souris (MeSH)</term>
<term>Système de signalisation des MAP kinases (MeSH)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>p38 Mitogen-Activated Protein Kinases (métabolisme)</term>
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<term>JNK Mitogen-Activated Protein Kinases</term>
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<term>TOR Serine-Threonine Kinases</term>
<term>p38 Mitogen-Activated Protein Kinases</term>
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<term>Jaagsiekte sheep retrovirus</term>
<term>Pulmonary Adenomatosis, Ovine</term>
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<term>Adénomatose pulmonaire ovine</term>
<term>Produits du gène env</term>
<term>Rétrovirus Jaagsiekte du mouton</term>
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<term>Jaagsiekte sheep retrovirus</term>
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<term>Pulmonary Adenomatosis, Ovine</term>
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<term>Extracellular Signal-Regulated MAP Kinases</term>
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<term>JNK Mitogen-Activated Protein Kinases</term>
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<term>Produits du gène env</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Rétrovirus Jaagsiekte du mouton</term>
<term>Sérine-thréonine kinases TOR</term>
<term>p38 Mitogen-Activated Protein Kinases</term>
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<term>Jaagsiekte sheep retrovirus</term>
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<term>Autophagy</term>
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<term>Immunotransfert</term>
<term>Interactions hôte-pathogène</term>
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<div type="abstract" xml:lang="en">The envelope (Env) of Jaagsiekte sheep retrovirus (JSRV) is an oncoprotein of ovine pulmonary adenocarcinoma (OPA). Autophagy is involved in different cancers, but how it is carcinogenic in JSRV Env is unclear. Modulation of autophagy in exJSRV-env-NM-transfected cells through the Akt/mTOR and MAPK signaling pathway was studied, and we observed strong positive labeling of p-Akt, p-mTOR, p-MEK1/2, p-ERK1/2, p-p38 and p-JNK in tumor cells and typical type II pneumocytes in naturally infected OPA lung tissues, which was co-aligned with JSRV-Env positive cells as shown by immunohistochemical and microscopic analysis. Akt/mTOR and MAPK pathways were activated in OPA lung and JSRV-Env transfected NIH 3T3 cells. Decreased Beclin1 and LC3 II/I suggested that autophagy was inhibited in OPA lung and JSRV-Env transfected NIH 3T3 cells. Beclin1 and LC3 II/I increased in JSRV-Env transfected NIH3T3 cells treated with mTOR inhibitor (rapamycin), ERK1/2 inhibitor (PD 98059), p38 inhibitor (SB 203580) and JNK inhibitor (SP 600125), suggesting that Akt/mTOR and MAPK pathways were responsible for JSRV-Env decreased autophagy. In conclusion, JSRV Env decreased autophagy in JSRV-Env transfected NIH3T3 cells through Akt/mTOR and MAPK pathways, in particular, JNK and p38 pathways.</div>
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<AbstractText>The envelope (Env) of Jaagsiekte sheep retrovirus (JSRV) is an oncoprotein of ovine pulmonary adenocarcinoma (OPA). Autophagy is involved in different cancers, but how it is carcinogenic in JSRV Env is unclear. Modulation of autophagy in exJSRV-env-NM-transfected cells through the Akt/mTOR and MAPK signaling pathway was studied, and we observed strong positive labeling of p-Akt, p-mTOR, p-MEK1/2, p-ERK1/2, p-p38 and p-JNK in tumor cells and typical type II pneumocytes in naturally infected OPA lung tissues, which was co-aligned with JSRV-Env positive cells as shown by immunohistochemical and microscopic analysis. Akt/mTOR and MAPK pathways were activated in OPA lung and JSRV-Env transfected NIH 3T3 cells. Decreased Beclin1 and LC3 II/I suggested that autophagy was inhibited in OPA lung and JSRV-Env transfected NIH 3T3 cells. Beclin1 and LC3 II/I increased in JSRV-Env transfected NIH3T3 cells treated with mTOR inhibitor (rapamycin), ERK1/2 inhibitor (PD 98059), p38 inhibitor (SB 203580) and JNK inhibitor (SP 600125), suggesting that Akt/mTOR and MAPK pathways were responsible for JSRV-Env decreased autophagy. In conclusion, JSRV Env decreased autophagy in JSRV-Env transfected NIH3T3 cells through Akt/mTOR and MAPK pathways, in particular, JNK and p38 pathways.</AbstractText>
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