Isorhamnetin Inhibits Proliferation and Invasion and Induces Apoptosis through the Modulation of Peroxisome Proliferator-activated Receptor ϒ Activation Pathway in Gastric Center

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Article on PPAR-γ, a nuclear transcription factor that plays a critical role in the development of gastric cancer.

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15 p.: ill.

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Ramachandran, Lalitha; Manu, Kanjoormana Aryan; Shanmugam, Muthu K.; Li, Feng; Siveen, Kodappully Sivaraman; Vali, Shireen et al. November 2, 2012.

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Article on PPAR-γ, a nuclear transcription factor that plays a critical role in the development of gastric cancer.

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15 p.: ill.

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Abstract: Background: PPAR-γ, a nuclear transcription factor, plays a critical role in the development of gastric cancer (GC). Hence, novel agents that can modulate PPAR-γ cascade have a great potential for the treatment of GC. Results: Isorhamnetin (IH) modulates PPAR-γ pathway in GC. Conclusion: IH induces apoptosis through the activation of the PPAR-γ pathway. Significance: The study proposes a novel agent for GC treatment.

A correction is included on the final page of this article. Published June 28, 2013, Journal of Biological Chemistry, Vol. 288, No. 26, pp. 18777.

Copyright © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.

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  • Journal of Biological Chemistry, 2012, Rockville: American Society for Biochemistry and Molecular Biology, pp. 38028-38040

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  • Publication Title: Journal of Biological Chemistry
  • Volume: 287
  • Issue: 45
  • Page Start: 38028
  • Page End: 38040
  • Peer Reviewed: Yes

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  • November 2, 2012

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  • May 7, 2014, 12:22 a.m.

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Ramachandran, Lalitha; Manu, Kanjoormana Aryan; Shanmugam, Muthu K.; Li, Feng; Siveen, Kodappully Sivaraman; Vali, Shireen et al. Isorhamnetin Inhibits Proliferation and Invasion and Induces Apoptosis through the Modulation of Peroxisome Proliferator-activated Receptor ϒ Activation Pathway in Gastric Center, article, November 2, 2012; [Rockville, Maryland]. (digital.library.unt.edu/ark:/67531/metadc284550/: accessed December 16, 2018), University of North Texas Libraries, Digital Library, digital.library.unt.edu; crediting UNT College of Arts and Sciences.