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RNAi against STAT3 Results in Cell Death in Human Bronchial Epithelial Cells Exposed to Cigarette Smoke Extract

Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska

Correspondence and requests for reprints should be addressed to Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68198. E-mail: xdliu{at}unmc.edu

Constitutive activation of STAT3 may contribute to carcinogenesis by preventing programmed cell death. Cigarette smoke can induce DNA damage without inducing apoptosis in human bronchial epithelial cells. Smoke induction of IL-6, which acts in an autocrine/paracrine manner, plays a key role in preventing apoptosis in response to cigarette smoke–induced DNA damage. Since IL-6 activates STAT3, the current study was designed to determine the role of STAT3 in modulating human bronchial epithelial cell survival in response to cigarette smoke exposure. To accomplish this, STAT3 phosphorylation, as well as DNA binding activity of STAT3 in response to cigarette smoke exposure, were assessed by immunoblot and electrophoretic mobility shift assay, respectively. In addition, normal human bronchial epithelial cells were exposed to cigarette smoke extract with and without transfection with siRNA specifically targeting STAT3 (SMARTpool; Dharmacon, Lafayette, CO). Cigarette smoke exposure resulted in STAT3 phosphorylation in a time- and concentration-dependent manner. Cigarette smoke also increased STAT3-DNA binding activity. Introduction of STAT3 siRNA significantly suppressed STAT3 expression and caused cell death in response to cigarette smoke exposure. These results suggest that STAT3 is activated by cigarette smoke and that the STAT3 signal pathway plays an important role in modulating survival or death in human bronchial epithelial cells exposed to cigarette smoke.

FOOTNOTES

Conflict of Interest Statement: X.L. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

(Received in original form March 20, 2006; accepted in final form March 28, 2006)

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