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Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
Published on: September 20, 2024
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PFOS promotes lung adenocarcinoma cell proliferation through PI3K/AKT/NF-κB mediated EMT
Ruijian Liu1, Qiuyu Yang1, Shanshan Fan1
1Guangdong Provincial Emergency Hospital, The Affiliated Guangdong Second Provincial General Hospital of Jinan University, 466 Middle Xingang Road, Guangzhou, 510317, Guangdong, People's Republic of China.
Summary
Perfluoroalkyl substances (PFASs) like PFOS promote lung cancer cell growth by inhibiting apoptosis and enhancing migration. This study reveals PFOS activates the PI3K/AKT/NF-κB pathway, contributing to lung adenocarcinoma development.
Area of Science:
- Environmental Health
- Toxicology
- Oncology
Background:
- Perfluoroalkyl and polyfluoroalkyl substances (PFASs) are widespread synthetic chemicals.
- Perfluorooctanesulfonic acid (PFOS) exposure is linked to health issues, but its role in lung cancer is unclear.
Purpose of the Study:
- Investigate PFOS effects on lung adenocarcinoma (LUAD) cell lines.
- Elucidate the carcinogenic mechanisms of PFOS in LUAD.
Main Methods:
- Evaluated PFOS-induced proliferation, anti-apoptotic properties, and epithelial-mesenchymal transition (EMT) in H1299 and A549 LUAD cells.
- Examined PI3K/AKT/NF-κB pathway activation and its role in apoptosis inhibition.
Main Results:
- PFOS significantly promoted LUAD cell growth by suppressing apoptosis.
- PFOS accelerated EMT, enhancing cell migration.
- PFOS activated the PI3K/AKT/NF-κB pathway, facilitating proliferation and migration.
Conclusions:
- PFOS exposure may exacerbate lung conditions or induce carcinogenesis.
- PFOS suppresses apoptosis and activates PI3K/AKT/NF-κB signaling in LUAD.
- Findings provide evidence for PFOS's carcinogenic potential in lung adenocarcinoma.
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