2013
DOI: 10.1186/1475-2867-13-38
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Independent of ErbB1 gene copy number, EGF stimulates migration but is not associated with cell proliferation in non-small cell lung cancer

Abstract: BackgroundLung cancer often exhibits molecular changes, such as the overexpression of the ErbB1 gene. ErbB1 encodes epidermal growth factor receptor (EGFR), a tyrosine kinase receptor, involved mainly in cell proliferation and survival. EGFR overexpression has been associated with more aggressive disease, poor prognosis, low survival rate and low response to therapy. ErbB1 amplification and mutation are associated with tumor development and are implicated in ineffective treatment. The aim of the present study … Show more

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Cited by 25 publications
(27 citation statements)
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“…Thus, our results suggest that constitutive activation of EGFR also contributes to basal migration in PC-9 cells. It has also been reported that EGFR activation by EGF resulted in morphological change and increase of cell migration in A549 and HK2 lung cancer cell lines [26]. Our results also indicate that the expression of P2X7 receptor in PC-9 cells is mediated by activation of the EGFR pathway.…”
Section: Discussionsupporting
confidence: 85%
“…Thus, our results suggest that constitutive activation of EGFR also contributes to basal migration in PC-9 cells. It has also been reported that EGFR activation by EGF resulted in morphological change and increase of cell migration in A549 and HK2 lung cancer cell lines [26]. Our results also indicate that the expression of P2X7 receptor in PC-9 cells is mediated by activation of the EGFR pathway.…”
Section: Discussionsupporting
confidence: 85%
“…Indeed, EGFR inhibition has been shown to reduce cell migration and wound healing in corneal (56) and intestinal (57) tissues, as well as in keratinocytes and non-small cell lung cancer (NSCLC) (58) cells. Similar to the results that we obtained with our epithelial carcinoma cell line, Lauand et al reported that inhibition of EGFR reduced migration but not the proliferation rate of epithelial NSCLC cells (58). Therefore, we propose that decreased cell-cell adhesion and increased EGFR activation likely contribute to the increased migratory phenotype of our pre-EMT cells.…”
Section: Discussionsupporting
confidence: 79%
“…Next, we investigated the EGFR copy number in each clone by quantitative PCR. Comparison with the normal human diploid cell line TIG-3 indicated that each clone carried nearly four copies of EGFR, while parental A549 cells had three copies as reported previously ( Fig 2D) [27]. From the results of the L858R mutation ratio ( Fig 2C) and EGFR copy number ( Fig 2D), clones 82-12, 47-3, and 73-4 were inferred to have one, two, and two copies of the L858R EGFR mutation, respectively (Fig 2E).…”
Section: Plos Onesupporting
confidence: 83%
“…For genome editing, we chose the CRISPR-Cas9D10A nickase (Cas9n) system, which minimizes off-target activity [23,24,26]. The human NSCLC cell line A549, which contains three copies of wild-type EGFR [27], was co-transfected with two EGFRtargeting Cas9n vectors and a ssODN (146 nucleotides, sense strand) donor containing a CTG!CGG mutation (boxed in Fig 1A) flanked by sequences homologous to the EGFR target site. Importantly, we synonymously mutated one nucleotide in the protospacer adjacent motif and five or six nucleotides in the 'seed' region (3 0 region) of the sense or anti-sense sgRNA sequence to prevent repetitive attack by Cas9n after successful integration of the exogenous sequence ( Fig 1A) [26].…”
Section: Design and Preparation Of Tools For Crispr-cas9 Genome Editingmentioning
confidence: 99%