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논문 기본 정보

자료유형
학술저널
저자정보
Sun, Guo-Gui (Department of Chemoradiotherapy, Tangshan People's Hospital) Hu, Wan-Ning (Department of Chemoradiotherapy, Tangshan People's Hospital) Wang, Ya-Di (Department of Radiotherapy, The Military General Hospital of Beijing PLA) Yang, Cong-Rong (Department of Radiotherapy, The Fourth Hospital of Hebei Medical University) Lu, Yi-Fang (Department of Endocrinology, Tangshan Workers Hospital)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제13권 제7호
발행연도
2012.1
수록면
3,015 - 3,023 (9page)

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The mitochondrial antioxidant protein manganese superoxide dismutase (MnSOD) may represent a new type of tumor suppressor protein. Overexpression of the cDNA of this gene by plasmid or recombinant lentiviral transfection in various types of cancer leads to growth suppression both in vitro and in vivo. We previously determined that changes in MnSOD expression had bidirectional effects on adriamycin (ADR) when combined with nitric oxide (NO). Radiation induces free radicals in a manner similar to ADR, so we speculated that MnSOD combined with NO would also have a bidirectional effect on cellular radiosensitivity. To examine this hypothesis, TE-1 human esophageal squamous carcinoma cells were stably transfected using lipofectamine with a pLenti6-DEST plasmid containing human MnSOD cDNA at moderate to high overexpression levels or with no MnSOD insert. Blastidicin-resistant colonies were isolated, grown, and maintained in culture. We found that moderate overexpression of MnSOD decreased growth rates, plating efficiency, and increased apoptosis. However, high overexpression increased growth rates, plating efficiency, and decreased apoptosis. When combined with NO, moderate overexpression of MnSOD increased the radiosensitivity of esophageal cancer cells, whereas high MnSOD overexpression had the opposite effect. This finding suggests a potential new method to kill certain radioresistant tumors and to provide radioresistance to normal cells.

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