Beclin1-induced Autophagy Abrogates Radioresistance of Lung Cancer Cells by Suppressing Osteopontin

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  • CHANG Seung-Hee
    Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University
  • MINAI-TEHRANI Arash
    Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University
  • SHIN Ji-Young
    Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University
  • PARK Sungjin
    Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University
  • KIM Ji-Eun
    Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University Department of Nanofusion Technology, Graduate School of Convergence Science and Technology, Seoul National University
  • YU Kyeong-Nam
    Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University
  • HONG Seong-Ho
    Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University
  • HONG Choong-Man
    Division of Medical Device Management, Osong Health Technology Administration Complex
  • LEE Kee-Ho
    Laboratory of Radiation Molecular Oncology, Korea Institute of Radiological and Medical Sciences
  • BECK Jr George R
    Division of Endocrinology, Metabolism and Lipids, Emory University School of Medicine
  • CHO Myung-Haing
    Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University Department of Nanofusion Technology, Graduate School of Convergence Science and Technology, Seoul National University Graduate Group of Tumor Biology, Seoul National University Center for Food Safety and Toxicology, Seoul National University National Institute of Food and Drug Safety Advanced Institute of Convergence Technology, Seoul National University

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Osteopontin (OPN) serves as an indicator of resistance to radiotherapy. However, the role of OPN in the development of acquired radioresistance in human lung cancer cells has not yet been fully elucidated. Therefore, the potential importance of OPN as a marker of lung cancer with a potential significant role in the development of radioresistance against repeated radiotherapy has prompted us to define the pathways by which OPN regulates lung cancer cell growth. In addition, autophagy has been reported to play a key role in the radiosensitization of cancer cells. Here, we report that increased OPN expression through induction of nuclear p53 following irradiation was inhibited by exogenous beclin-1 (BECN1). Our results clearly show that BECN1 gene expression led to induction of autophagy and inhibition of cancer cell growth and angiogenesis. Our results suggest that the induction of autophagy abrogated the radioresistance of the cancer cells. Interestingly, we showed that knockdown of OPN by lentivirus-mediated shRNA induced the autophagy of human lung cancer cell. Taken together, these results suggest that OPN and BECN1 can be molecular targets for overcoming radioresistance by controlling autophagy.

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