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Cited by 69HER2/EGFR in Cancer ResearchLung Cancer Treatments and MutationsCarcinogens and Genotoxicity Assessment

Benzo[a]pyrene promotes proliferation of human lung cancer cells by accelerating the epidermal growth factor receptor signaling pathway

Kometani, Takuro, Yoshino, Ichiro, Miura, Naoko, Okazaki, Hiroshi, Ohba, Taro, Takenaka, Tomoyoshi, Shoji, Fumihiro, Yano, Tokujiro +1 more·2009·Cancer Letters
DOI 10.1016/j.canlet.2008.12.017
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Abstract

Smoking is an independent prognostic factor of lung adenocarcinoma. Benzo[a]pyrene (B[a]P) is one of the strongest carcinogens and it is present in both the environment and cigarette smoke. In this study, the effect of B[a]P on the proliferative activity of lung adenocarcinoma cells was investigated. A lung adenocarcinoma cell line, A549, was cultured with B[a]P for various periods, and its proliferative activity was examined by an MTS assay. To investigate the intracellular events related to the proliferative activity, the gene expression profile was investigated by a microarray analysis and a quantitative RT-PCR, and the protein expression and activation status of Akt, ERK 1/2 and the epidermal growth factor receptor (EGFR) were examined by a western blot analysis. Following the culture with B[a]P for 24 weeks, the serum-independent proliferative activity was increased. A microarray analysis revealed that a reversible upregulation of the EGFR and epiregulin genes was recognized in the B[a]P treated cells, in which the overexpression of the phosphorylated EGFR protein was also recognized. The EGFR tyrosine kinase inhibitor reduced the cellular proliferation and the level of phosphorylation of ERK1/2, which is a downstream signal of the EGFR, in the B[a]P-treated A549 cells. Moreover, the B[a]P treatment increased the mRNA expressions of the ligands for EGFR such as amphiregulin and epiregulin. B[a]P increases the proliferative potential of lung adenocarcinoma cells through the EGFR signaling pathway.

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Crossref · 10.1016/j.canlet.2008.12.017

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  • Carcinogenic species participating in ROS formation may trigger overexpression of phosphorylated EGFR protein and its ligand amphiregulin (AREG), which promotes uncontrolled proliferation of lung adenocarcinoma cells.

    “Carcinogenic species participating in ROS formation may trigger overexpression of the phosphorylated epidermal growth factor receptor (EGFR) protein and its ligand amphiregulin (AREG) a widely expressed transmembrane tyrosine kinase which in turn promotes uncontrolled proliferation of lung adenocarcinoma cells (Kometani et al. 2009).”

    From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Kometani et al. 2009

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Authors
Kometani, T., Yoshino, I., Miura, N., Okazaki, H., Ohba, T., Takenaka, T., Shoji, F., Yano, T., & Maehara, Y.
Affiliations
  • Kyushu University (JP)
  • Chiba University (JP)
Corresponding author
Kometani, Takuro
ORCID
Venue
Cancer Letters
Publisher
Elsevier BV
Published
2009-06
Volume
278
Issue
1
Pages
27-33
ISSN
0304-3835 (ISSN-L)
DOI
10.1016/j.canlet.2008.12.017
OpenAlex
W2056347472
Cited by
69
References
33
Citations by year
2026: 2 · 2025: 6 · 2024: 4 · 2023: 6 · 2022: 7 · 2021: 4 · 2020: 1 · 2019: 5 · 2018: 4 · 2017: 4 · 2016: 5 · 2015: 4 · 2014: 2 · 2013: 3 · 2012: 3
FWCI
2.00
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Cancer Letters (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
Keywords
benzo[a]pyrene, lung adenocarcinoma, cell proliferation, epidermal growth factor receptor, EGFR signaling, epiregulin, amphiregulin, ERK1/2, Akt, tobacco smoke carcinogens, A549 cells, EGFR tyrosine kinase inhibitors
MeSH terms
Gefitinib, Adenocarcinoma, Antineoplastic Agents, Benzo(a)pyrene, Cell Division, Humans, Lung Neoplasms, Quinazolines, RNA, Messenger, RNA, Neoplasm, Signal Transduction, Gene Expression Regulation, Neoplastic, Cell Culture Techniques, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Cell Proliferation, ErbB Receptors

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