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The Role of Visfatin-Notch Signaling Axis During the Apoptosis of Human Breast Cancer Cells

초록

영어

Adipokines play an important role in obesity-related metabolic disorders which is favorable for breast cancer risk. Visfatin has recently been identified as a novel visceral adipokine. However, the role of visfatin in human breast cancer has not been fully understood. Here, we investigated the expressional pattern of visfatin in the process of apoptosis of human breast cancer cells MDA-MB-231 induced by visin (tentative name: visfatininhibitor). Visin caused the apoptosis of MDA-MB-231 cells as determined by MTT assay and FACS analysis. The expression of Bcl-2 and Bcl-xL that are essential for cell growth and survival was apparently attenuated after visin
treatment. In addition, the levels of visfatin mRNA and protein were downregulated by visin. Furthermore, the silencing of visfatin expression by siRNA has been shown to inhibit the cell viability and growth, which was enhanced by the treatment of visin. We next focused on the regulation of Notch-1 gene expression because Notch-1 has been well known to play crucial roles in the survival and proliferation of breast cancer cells. Similar to visfatin, Notch-1 levels were downregulated by visin treatment. Furthermore, the transfection of MDA-MB-231 cells with a visfatin siRNA resulted in the reduction of Notch-1 gene expression levels. Taken together, our results suggest that visfatin-Notch-1 signaling axis may contribute to the survival of breast cancer cells.

저자정보

  • Su-Ryun KIM Department of Physiology, School of Medicine, Medical Research Center for Ischemic Tissue Regeneration, Pusan National University Medical Science Education Center (BK21 Program), Pusan National University, Yangsan, 626-770, South Korea.
  • Seon Yeong PARK Department of Physiology, School of Medicine, Medical Research Center for Ischemic Tissue Regeneration, Pusan National University Medical Science Education Center (BK21 Program), Pusan National University, Yangsan, 626-770, South Korea.
  • Jee-Young KIM Department of Physiology, School of Medicine, Medical Research Center for Ischemic Tissue Regeneration, Pusan National University Medical Science Education Center (BK21 Program), Pusan National University, Yangsan, 626-770, South Korea.
  • Young-soon KANG Department of Physiology, School of Medicine, Medical Research Center for Ischemic Tissue Regeneration, Pusan National University Medical Science Education Center (BK21 Program), Pusan National University, Yangsan, 626-770, South Korea.
  • Moon-Kyoung BAE Department of Oral Physiology, School of Dentistry, Pusan National University, Yangsan, 626-770, South Korea.
  • Soo-Kyung BAE Department of Physiology, School of Medicine, Medical Research Center for Ischemic Tissue Regeneration, Pusan National University Medical Science Education Center (BK21 Program), Pusan National University, Yangsan, 626-770, South Korea.

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