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(American Journal of Pathology. 2006;168:1345-1353.)
© 2006 American Society for Investigative Pathology

Aquaporin 1 Is Overexpressed in Lung Cancer and Stimulates NIH-3T3 Cell Proliferation and Anchorage-Independent Growth

Mohammad Obaidul Hoque^*, Jean-Charles Soria, Janghee Woo^*, Taekyeol Lee^*, Juna Lee^*, Se Jin Jang, Sunil Upadhyay^*, Barry Trink^*, Constance Monitto^*, Chantal Desmaze, Li Mao^¶, David Sidransky^*|| and Chulso Moon^*||

From the Departments of Otolaryngology–Head and Neck Surgery,^* Anesthesiology and Critical Care Medicine, and Oncology, and the Sidney Kimmel Comprehensive Cancer Center,^|| Johns Hopkins University School of Medicine, Baltimore, Maryland; the Department of Thoracic/Head and Neck Medical Oncology,^¶ Molecular Biology Laboratory, The University of Texas M. D. Anderson Cancer Center, Houston, Texas; the Division of Cancer Medicine, Gustave Roussy Institute, Villejuif, France; and the Department of Pathology, Asan Medical Center, College of Medicine, Ulsan University, Seoul, Korea

The aquaporins represent a family of transmembrane water channel proteins that play a major role in trans-cellular and transepithelial water movement. Most tumors have been shown to exhibit high vascular permeability and interstitial fluid pressure, but the transport pathways for water within tumors remain unknown. Here, we tested 10 non-small cell lung cancer cell lines of various origins by reverse transcriptase-polymerase chain reaction and Western blot analysis and identified clear expression of aquaporin 1 (AQP1) in seven cell lines. We next examined the distribution of the AQP1 protein in several types of primary lung tumors (16 squamous cell carcinomas, 21 adenocarcinomas, and 7 bronchoalveolar carcinomas) by immunohistochemical staining. AQP1 was overexpressed in 62% (13 of 21) and 75% (6 of 8) of adenocarcinoma and bronchoalveolar carcinoma, respectively, whereas all cases of squamous cell carcinoma and normal lung tissue were negative. Forced expression of full-length AQP1 cDNA in NIH-3T3 cells induced many phenotypic changes characteristic of transformation, including cell proliferation-enhancing activity by the MTT assay and anchorage-independent growth in soft agar. Although further details on the molecular function of AQP1 related to tumorigenesis remain to be elucidated, our results suggest a potential role of AQP1 as a novel therapeutic target for the management of lung cancer.

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