Abstract | BACKGROUND: METHODS: EGFR over-expression and three EFGR-mutant (EGFR-E746-A750del, EGFR-T790M and EGFR-L858R) plasmid were designed and transfected H1299 cells with Lipofectamine 2000. H1299 cells transfected with empty vector were negative control (NC), and H1299 cells without transfection were set as blank control (BC). The effects of EGFR over-expression and mutations on the proliferation, migration and invasion of H1299 cells were detected by cell cloning assay, wound healing assay and Transwell assay. The mRNA and protein expression levels of MMP-2, MMP-9, CXCR4 and CXCL12 were detected by RT-PCR and Western blot. RESULTS: Compared with negative control group and blank control group, EGFR over-expression and EGFR-E746-A750 deletion have significantly higher colony formation (28±2, 28.33±4.16; respectively) (P<0.05) and the cell migration and invasion ability were significantly increased (P<0.05). RT-PCR and Western blot assay showed that the mRNA and protein expression of MMP-2, MMP-9, CXCR4 and CXCL12 in EGFR over-expression and EGFR-E746-A750 deletion group were remarkably higher than that in negative control and blank control group (P<0.05). CONCLUSIONS: EGFR over-expression and 19 exon deletion can promote the expression of MMP-2 and MMP-9 by up-regulating CXCR4/CXCL12 signaling pathway, leading to the change of tumor biological characteristics such as higher proliferation, migration and invasion ability.
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Authors | Jia Feng, Xueyan Wei, Chuang Li, Mingxiong Guo, Min Peng, Qibin Song, Guang Han |
Journal | Zhongguo fei ai za zhi = Chinese journal of lung cancer
(Zhongguo Fei Ai Za Zhi)
Vol. 21
Issue 7
Pg. 503-512
(Jul 20 2018)
ISSN: 1999-6187 [Electronic] China |
PMID | 30037369
(Publication Type: Journal Article)
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Chemical References |
- CXCL12 protein, human
- CXCR4 protein, human
- Chemokine CXCL12
- Receptors, CXCR4
- ErbB Receptors
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Topics |
- Adenocarcinoma
(pathology)
- Adenocarcinoma of Lung
- Cell Line, Tumor
- Cell Movement
(genetics)
- Chemokine CXCL12
(metabolism)
- ErbB Receptors
(genetics)
- Gene Expression Regulation, Neoplastic
- Humans
- Lung Neoplasms
(pathology)
- Mutation
- Neoplasm Invasiveness
- Receptors, CXCR4
(metabolism)
- Signal Transduction
(genetics)
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