ArticleInternational journal of clinical and experimental pathology2018
Targeting ROR1 inhibits epithelial to mesenchymal transition in human lung adenocarcinoma via mTOR signaling pathway.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- A Small Molecule Targeting the Intracellular Tyrosine Kinase Domain of ROR1 (KAN0441571C) Induced Significant Apoptosis of Non-Small Cell Lung Cancer (NSCLC) Cells.Pharmaceutics · 2023Article
- Tumor-associated macrophages mediate resistance of EGFR-TKIs in non-small cell lung cancer: mechanisms and prospects.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The receptor tyrosine kinase-like orphan receptor 1 (ROR1) is a type I surface transmembrane protein that contributes to progression of tumor-cell growth and metastasis. We and others have shown that the roles of ROR1 include inhibiting apoptosis, potentiating EGFR signaling, and inducing proliferation in lung cancer, but the roles and mechanisms of ROR1 in lung adenocarcinoma metastasis have not been elucidated. Here we chose four lung adenocarcinoma cell lines, PC9 (erlotinib-sensitive), PC9erlo (acquired erlotinib-resistant), NCI-H358 (partial erlotinib-resistant), and NCI-H1975 (erlotinib-resistant) as cell models to simulate the clinical situation. We found that ROR1 prompted epithelial to mesenchymal transition (EMT) by increasing the expression level of a key epithelial gene, E-cadherin, while decreasing the expression level of the key mesenchymal gene vimentin. Silencing ROR1 by siRNA significantly reduced the migration and invasion of lung adenocarcinoma cells in
Indexed as
Identifiers
31949551PMC6962910W3013388971What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.