본문 바로가기
HOME> 논문 > 논문 검색상세

논문 상세정보

Biochemical and biophysical research communications v.494 no.3/4, 2017년, pp.706 - 713   SCI SCIE
본 등재정보는 저널의 등재정보를 참고하여 보여주는 베타서비스로 정확한 논문의 등재여부는 등재기관에 확인하시기 바랍니다.

Galangin enhances TGF-β1-mediated growth inhibition by suppressing phosphorylation of threonine 179 residue in Smad3 linker region

Kwak, Mi-Kyung (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Seoul National University, Suwon, Kyunggi-do 16229, Republic of Korea ); Yang, Kyung-Min (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Seoul National University, Suwon, Kyunggi-do 16229, Republic of Korea ); Park, Jinah (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Seoul National University, Suwon, Kyunggi-do 16229, Republic of Korea ); Lee, Siyoung (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Seoul National University, Suwon, Kyunggi-do 16229, Republic of Korea ); Park, Yuna (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Seoul National University, Suwon, Kyunggi-do 16229, Republic of Korea ); Hong, Eunji (Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Seoul National University, Suwon, Kyunggi-do 16229, Republic of Korea ); Sun, Eun Jin (Precision Medicine Research Center, Advanced Institutes of Convergence ); An, Haein ( ); Park, Sujin ( ); Pang, Kyoungwha ( ); Lee, Jihee ( ); Kang, Jin Muk ( ); Kim, Pyunggang ( ); Ooshima, Akira ( ); Kim, Seong-Jin ( );
  • 초록  

    Abstract Smad3 linker phosphorylation is a candidate target for several kinases that play important roles in cancer cell initiation, proliferation and progression. Also, Smad3 is an essential intracellular mediator of TGF-β1-induced transcriptional responses during carcinogenesis. Therefore, it is highly advantageous to identify and develop inhibitors targeting Smad3 linker phosphorylation for the treatment of cancers. Galangin (3,5,7-trihydroxyflavone) has been known to be an active flavonoid showing a cytotoxic effect on several cancer cells. However, the mechanism of action of galangin in various cancers remains unclear, and there has been no report concerning regulation of Smad3 phosphorylation by galangin. In the present study, we show that galangin significantly induced apoptosis and inhibited cell proliferation in the presence of TGF-β1 in both human prostate and pancreatic cancer cell lines. Particularly, galangin effectively inhibits phosphorylation of the Thr-179 site at Smad3 linker region through suppression of CDK4 phosphorylation. Thus, galangin can be a promising candidate as a selective inhibitor to suppress phosphorylation of Smad3 linker region. Highlights Galangin significantly induced apoptosis in the presence of TGF-β1. Galangin inhibits phosphorylation of the Thr-179 site at the Smad3 linker region. Galangin suppresses CDK4-mediated Smad3 linker phosphorylation.


  • 주제어

    Galangin .   Smad3 linker phosphorylation .   TGF-β1 .   Prostate cancer .   Pancreatic cancer.  

 활용도 분석

  • 상세보기

    amChart 영역
  • 원문보기

    amChart 영역

원문보기

무료다운로드
  • 원문이 없습니다.
유료다운로드

유료 다운로드의 경우 해당 사이트의 정책에 따라 신규 회원가입, 로그인, 유료 구매 등이 필요할 수 있습니다. 해당 사이트에서 발생하는 귀하의 모든 정보활동은 NDSL의 서비스 정책과 무관합니다.

원문복사신청을 하시면, 일부 해외 인쇄학술지의 경우 외국학술지지원센터(FRIC)에서
무료 원문복사 서비스를 제공합니다.

NDSL에서는 해당 원문을 복사서비스하고 있습니다. 위의 원문복사신청 또는 장바구니 담기를 통하여 원문복사서비스 이용이 가능합니다.

이 논문과 함께 출판된 논문 + 더보기