Napsin A is negatively associated with EMT‑mediated EGFR‑TKI resistance in lung cancer cells.

No abstract is available for this paper.

• Publication year

  2018

• Venue

  Molecular Medicine Reports

• Publication date

  2018-08-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.3892/mmr.2018.9075PMID 29845258
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• EGFR-mutated oncogene-addicted non-small cell lung cancer: current trends and future prospects.

  2012cited by this paper
• First-line treatment of EGFR-mutant non-small-cell lung cancer: the role of erlotinib and other tyrosine kinase inhibitors

  2012cited by this paper
• Secrets of Drug Resistance in NSCLC Exposed by New Molecular Definition of EMT

  2012cited by this paper
• Epithelial-mesenchymal transition in EGFR-TKI acquired resistant lung adenocarcinoma.

  2010cited by this paper
• TGF-β IL-6 axis mediates selective and adaptive mechanisms of resistance to molecular targeted therapy in lung cancer

  2010cited by this paper
• Epithelial-mesenchymal transitions in development and disease.

  2009cited by this paper
• Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic.

  2009cited by this paper
• The aspartic protease napsin A suppresses tumor growth independent of its catalytic activity

  2008cited by this paper
• Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis.

  2008cited by this paper
• The role of epithelial-mesenchymal transition in cancer pathology.

  2007cited by this paper
• SPARC represses E-cadherin and induces mesenchymal transition during melanoma development.

  2006cited by this paper
• Epithelial to mesenchymal transition is a determinant of sensitivity of non-small-cell lung carcinoma cell lines and xenografts to epidermal growth factor receptor inhibition.

  2005cited by this paper
• KRAS Mutations and Primary Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib

  2005cited by this paper
• Napsin A is useful to distinguish primary lung adenocarcinoma from adenocarcinomas of other organs.

  2005cited by this paper
• Processing of Pulmonary Surfactant Protein B by Napsin and Cathepsin H*

  2004cited by this paper
• N-Cadherin Expression and Epithelial-Mesenchymal Transition in Pancreatic Carcinoma

  2004cited by this paper
• Aspartic proteinase napsin is a useful marker for diagnosis of primary lung adenocarcinoma

  2003cited by this paper
• Diverse cellular and molecular mechanisms contribute to epithelial plasticity and metastasis

  2003cited by this paper
• Usefulness of TA02 (napsin A) to distinguish primary lung adenocarcinoma from metastatic lung adenocarcinoma.

  2003cited by this paper
• Involvement of Napsin A in the C- and N-terminal Processing of Surfactant Protein B in Type-II Pneumocytes of the Human Lung*

  2003cited by this paper
• Integrins: bidirectional, allosteric signaling machines.

  2002cited by this paper
• Signal transduction by cell adhesion receptors and the cytoskeleton: functions of integrins, cadherins, selectins, and immunoglobulin-superfamily members.

  2002cited by this paper
• The Focal Adhesion Kinase‐‐A Regulator of Cell Migration and Invasion

  2002cited by this paper
• Focal Adhesion Kinase Activates Stat1 in Integrin-mediated Cell Migration and Adhesion*

  2001cited by this paper
• Integrin beta 1 signaling is necessary for transforming growth factor-beta activation of p38MAPK and epithelial plasticity.

  2001cited by this paper
• Inhibition of focal adhesion kinase expression or activity disrupts epidermal growth factor-stimulated signaling promoting the migration of invasive human carcinoma cells.

  2001cited by this paper
• Pre-clinical validation of a novel, highly sensitive assay to detect PML-RARalpha mRNA using real-time reverse-transcription polymerase chain reaction.

  2001cited by this paper
• Human Tissue Distribution of TA02, Which is Homologous with a New Type of Aspartic Proteinase, Napsin A

  2000cited by this paper
• FAK integrates growth-factor and integrin signals to promote cell migration

  2000cited by this paper
• Napsin A, a member of the aspartic protease family, is abundantly expressed in normal lung and kidney tissue and is expressed in lung adenocarcinomas

  1999cited by this paper
• Human napsin A: expression, immunochemical detection, and tissue localization

  1999cited by this paper
• Required role of focal adhesion kinase (FAK) for integrin-stimulated cell migration.

  1999cited by this paper
• Napsins: new human aspartic proteinases

  1998cited by this paper
• RGD and other recognition sequences for integrins.

  1996cited by this paper

• Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators

  2025cites this paper
• Revealing NAPSA's role in ccRCC: Insights from single-cell RNA sequencing.

  2025cites this paper
• Candidate pathway analysis of surfactant proteins identifies CTSH and SFTA2 that influences lung cancer risk.

  2023cites this paper
• Significance of thyroid transcription factor 1 and Napsin A for prompting the status of EGFR mutations in lung adenocarcinoma patients

  2022influential citation
• The role of radiotherapy-related autophagy genes in the prognosis and immune infiltration in lung adenocarcinoma

  2022cites this paper
• Napsin A Expression in Human Tumors and Normal Tissues

  2021influential citation
• Surfactant Expression Defines an Inflamed Subtype of Lung Adenocarcinoma Brain Metastases that Correlates with Prolonged Survival

  2020cites this paper