TACE/ADAM-17 Phosphorylation by PKC-Epsilon Mediates Premalignant Changes in Tobacco Smoke-Exposed Lung Cells
2011

Tobacco Smoke and Lung Cell Changes

publication 10 minutes Evidence: moderate

Author Information

Author(s): Lemjabbar-Alaoui Hassan, Sidhu Sukhvinder S., Mengistab Aklilu, Gallup Marianne, Basbaum Carol

Primary Institution: University of California San Francisco

Hypothesis

How does tobacco smoke induce TACE activation and hyperproliferation in lung cells?

Conclusion

Tobacco smoke induces TACE activation and hyperproliferation of lung cells through a signaling pathway involving PKCε and ROS.

Supporting Evidence

  • Tobacco smoke exposure leads to increased TACE phosphorylation.
  • PKCε is identified as the key isoform mediating TACE activation.
  • ROS are required for the activation of PKC and subsequent TACE activity.
  • Hyperproliferation of lung cells is linked to EGFR activation via TACE.

Takeaway

When tobacco smoke hits lung cells, it causes changes that can lead to cancer by making certain proteins more active.

Methodology

Lung epithelial cells were exposed to tobacco smoke, and TACE activity and phosphorylation were measured.

Limitations

The study primarily used a cell line, which may not fully represent in vivo conditions.

Statistical Information

P-Value

p<0.01

Statistical Significance

p<0.01

Digital Object Identifier (DOI)

10.1371/journal.pone.0017489

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