RETRACTED ARTICLE: Shp2 positively regulates cigarette smoke-induced epithelial mesenchymal transition by mediating MMP-9 production
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Dossier post-publication
- Nature
- Retraction
- Motif
- Concerns/Issues about Image;Duplication of/in Image;Investigation by Journal/Publisher;Manipulation of Images;Unreliable Results and/or Conclusions;Upgrade/Update of Prior Notice(s);
- Date
- 8/11/2023 0:00
- Signalé par OpenAlex ?
- Oui
Source : Retraction Watch, jointe par DOI. OpenAlex consigne la rétractation dans is_retracted, un booléen sur un espace d'états à au moins quatre valeurs ; il ne peut donc exprimer ni une expression de préoccupation, ni une correction, ni un rétablissement, et les rapporte comme false, ce qui se lit comme « rien à signaler ».
Résumé
Cigarette smoke (CS) is a major risk factor for the development of lung cancer and chronic obstructive pulmonary disease (COPD). Epithelial-mesenchymal transition (EMT) commonly coexists in lung cancer and COPD. CS triggers many factors including matrix metalloproteinases (MMPs) production, contributing to EMT progression in the lungs. Here, how Shp2 signaling regulates the CS-induced MMP-9 production and EMT progression were investigated in mouse lungs and in pulmonary epithelial cell cultures (NCI-H292) found CS induced MMP-9 production, EMT progression (increased vimentin and α-SMA; decreased E-cadherin) and collagen deposition in lung tissues; cigarette smoke extract (CSE) induced MMP-9 production and EMT-related phenotypes in NCI-H292 cells, which were partially prevented by Shp2 KO/KD or Shp2 inhibition. The CSE exposure induced EMT phenotypes were suppressed by MMP-9 inhibition. Recombinant MMP-9 induced EMT, which was prevented by MMP-9 inhibition or Shp2 KD/inhibition. Mechanistically, CS and CSE exposure resulted in ERK1/2, JNK and Smad2/3 phosphorylation, which were suppressed by Shp2 KO/KD/inhibition. Consequentially, the CSE exposure-induced MMP-9 production and EMT progression were suppressed by ERK1/2, JNK and Smad2/3 inhibitors. Thus, CS induced MMP-9 production and EMT resulted from activation of Shp2/ERK1/2/JNK/Smad2/3 signaling pathways. Our study contributes to the underlying mechanisms of pulmonary epithelial structural changes in response to CS, which may provide novel therapeutic solutions for treating associated diseases, such as COPD and lung cancer.
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La notice
- Revue
- Respiratory Research
- Thématique
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Domaine
- Medicine
- Établissements canadiens
- —
- Organismes subventionnaires
- University of California, San DiegoNankai UniversityNational Natural Science Foundation of ChinaYork UniversityZhejiang UniversityUniversity of Cincinnati
- Mots-clés
- Epithelial–mesenchymal transitionMatrix metalloproteinaseVimentinCancer researchLung cancerCOPDMedicineLungChemistrySignal transductionPhosphorylationCancerImmunologyPathologyInternal medicineMetastasisImmunohistochemistryBiochemistry
- Résumé présent dans OpenAlex
- oui