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      Cucurbitacin B and cucurbitacin I suppress adipocyte differentiation through inhibition of STAT3 signaling.

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          Abstract

          Cucurbitacin B, a member of the cucurbitaceae family, can act as a STAT3 signaling inhibitor to regulate the growth of hepatocellular carcinoma. STAT3 signaling has been shown to inhibit adipocyte differentiation through C/EBPα and PPARγ. Based on these studies, we hypothesized that cucurbitacin B would prevent PPARγ mediated adipocyte differentiation through STAT3 signaling. To test this hypothesis, mesenchymal C3H10T1/2 and 3T3-L1 preadipocyte cells were treated with a sub-cytotoxic concentration of cucurbitacin B. Cucurbitacin B treatment inhibits lipid accumulation and expression of adipocyte markers including PPARγ and its target genes in a dose-dependent manner. Cucurbitacin B treatment impairs STAT3 signaling as manifested by reduced phosphorylation of STAT3 and suppression of STAT3 target gene expression in preadipocytes. The anti-adipogenic effects of cucurbitacin B are significantly blunted in cells with STAT3 silenced by introducing small interfering RNA. Finally, our data show that cucurbitacin I, another cucurbitacin family member, also inhibits adipocyte differentiation by suppressing STAT3 signaling. Together, our data suggest the possibility of utilizing cucurbitacins as a new strategy to treat metabolic diseases and implicate STAT3 as a new target for the development of functional foods and drugs.

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          Author and article information

          Journal
          Food Chem. Toxicol.
          Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
          1873-6351
          0278-6915
          Feb 2014
          : 64
          Affiliations
          [1 ] Department of Food Science and Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
          [2 ] College of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 500-712, Republic of Korea.
          [3 ] School of Pharmacy, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
          [4 ] Department of Genetic Engineering, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
          [5 ] Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 440-746, Republic of Korea.
          [6 ] Functional Food Center, Korea Institute of Science and Technology, Gangneung Institute, Gangwon-do 210-340, Republic of Korea.
          [7 ] Department of Horticulture, Sunchon National University, 413 Jungangno, Suncheon, Jeonnam 540-742, Republic of Korea.
          [8 ] Department of Food Science and Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea. Electronic address: kwpark@skku.edu.
          Article
          S0278-6915(13)00802-8
          10.1016/j.fct.2013.11.040
          24316209
          9bc29b2b-fc6d-427c-b16a-e75d37abdd36
          Copyright © 2013 Elsevier Ltd. All rights reserved.
          History

          Adipocyte differentiation,Cucurbitacin B,Cucurbitacin I,PPARγ,STAT3

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