ArticleOncology reports2017
Benzo(a)pyrene enhances the EMT-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1.
Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The transcription factor TSHZ3 promotes tumor immunosuppression and inhibits metastasis in lung adenocarcinoma.Frontiers in immunology · 2025Article
- Arsenic and Benzo[a]pyrene Co-exposure Effects on MDA-MB-231 Cell Viability and Migration.Biological trace element research · 2025Article
- Role and mechanism of benzo[a]pyrene in the transformation of chronic obstructive pulmonary disease into lung adenocarcinoma.Journal of cancer research and clinical oncology · 2023Article
- Progesterone/Org inhibits lung adenocarcinoma cell growth via membrane progesterone receptor alpha.Thoracic cancer · 2020Article
- Gastrin-releasing peptide induces fibrotic response in MRC5s and proliferation in A549s.Cell communication and signaling : CCS · 2020Article
- FOXF2 acts as a crucial molecule in tumours and embryonic development.Cell death & disease · 2020Review
- Benzo[a]pyrene Perturbs Mitochondrial and Amino Acid Metabolism in Lung Epithelial Cells and Has Similar Correlations With Metabolic Changes in Human Serum.Journal of occupational and environmental medicine · 2019Article
- Emodin inhibits pancreatic cancer EMT and invasion by up‑regulating microRNA‑1271.Molecular medicine reports · 2018Article
- Article
- Molecular insights: Suppression of EGFR and AKT activation by a small molecule in non-small cell lung cancer.Genes & cancer · 2017Article
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Authors and funding
7 authors.
Funding
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Abstract
Benzo(a)pyrene (BaP), an important toxic component of cigarette smoke, can cause lung cancer and lead to the progression of lung cancer. In the present study, we investigated the effect of BaP on the migration of lung adenocarcinoma A549 cells. BaP (1 µM) promoted the migration of A549 cells in a time-dependent manner and upregulated the expression of the Twist family BHLH transcription factor 1 (Twist1). BaP also induced upregulation of the mesenchymal markers N-cadherin and vimentin and downregulation of the epithelial marker E-cadherin. When the expression of Twist1 was knocked down in A549 cells that were treated with BaP for 4 weeks (A549BaP-4w), the expression of Twist1 decreased, which inhibited the migration capacity of A549BaP-4w cells, the expression of N-cadherin and vimentin was downregulated and the expression of E-cadherin was upregulated. In addition, morphological observations of A549BaP-4w cells revealed that the epithelial characteristics of A549 cells became mesenchymal characteristics. When the expression of Twist1 was knocked down, the A549BaP-4w cells were transformed back to cells with epithelial characteristics. In conclusion, the results from the present study indicate that BaP enhances the epithelial-mesenchymal transition-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1.
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