ArticleCell adhesion & migration2019
BECN1 promotes the migration of NSCLC cells through regulating the ubiquitination of Vimentin.
Article in Cell adhesion & migration, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- USP14 promotes epithelial-mesenchymal transition and functions as a multifaceted biomarker in lung adenocarcinoma.Discover oncology · 2026Article
- Mechanistic Insights and Therapeutic Potentials of Ubiquitin-Proteasome System in Non-Small Cell Lung Cancer.Cell proliferation · 2025Review
- Targeting NLRC4 for potential therapeutic strategies in lung adenocarcinoma.Discover oncology · 2025Article
- Targeting autophagy and beyond: Deconvoluting the complexity of Beclin-1 from biological function to cancer therapy.Acta pharmaceutica Sinica. B · 2023Review
- UCHL3 promotes hepatocellular carcinoma cell migration by de-ubiquitinating and stabilizing Vimentin.Frontiers in oncology · 2023Article
- Pathophysiological Role of Vimentin Intermediate Filaments in Lung Diseases.Frontiers in cell and developmental biology · 2022Review
- Impact of Vimentin on Regulation of Cell Signaling and Matrix Remodeling.Frontiers in cell and developmental biology · 2022Review
- Design, Synthesis, and Biological Evaluation of Benzo[cd]indol-2(1H)-ones Derivatives as a Lysosome-Targeted Anti-metastatic Agent.Frontiers in oncology · 2021Article
- Efficacy and safety of S-1 maintenance therapy in advanced non-small-cell lung cancer patients.World journal of clinical cases · 2020Article
- The Roles of Beclin 1 Expression in Gastric Cancer: A Marker for Carcinogenesis, Aggressive Behaviors and Favorable Prognosis, and a Target of Gene Therapy.Frontiers in oncology · 2020Article
- Autophagy and pulmonary disease.Therapeutic advances in respiratory diseaseReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BECN1/Beclin1 is one of the key proteins in autophagy regulation. However, the biological functions of BECN1 in non-small cell lung cancer (NSCLC) were obscure. Here, we found that neither BECN1 knockdown nor overexpression affected the proliferation of NSCLC cells. Surprisingly, BECN1 overexpression increased cell migration and knocking down BECN1 significantly reduced the migratory ability of NSCLC cells. We further demonstrated that BECN1 could interact with Vimentin and affected its K48-linked ubiquitination. What's more, BECN1 could also interact with ubiquitin-specific peptidase 14 (USP14), the key de-ubiquitinase of Vimentin, and regulated USP14 mediated de-ubiquitination of Vimentin. Thus, our studies revealed an oncosupportive role of BECN1 in the migration of NSCLC cells through regulating the ubiquitination of Vimentin.
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