The anticancer effect of (1S,2S,3E,7E,11E)-3,7,11, 15-cembratetraen-17,2-olide(LS-1) through the activation of TGF-β signaling in SNU-C5/5-FU, fluorouracil-resistant human colon cancer cells

Marine Drugs
Eun-Ji KimHee-Kyoung Kang

Abstract

The anticancer effect of (1S,2S,3E,7E,11E)-3,7,11,15-cembratetraen-17,2-olide (LS-1) from Lobophytum sp. has been already reported in HT-29 human colorectal cancer cells. In this study, we examined the effect of LS-1 on the apoptosis induction of SNU-C5/5-FU, fluorouracil-resistant human colon cancer cells. Furthermore, we investigated whether the apoptosis-induction effect of LS-1 could arise from the activation of the TGF-β pathway. In SNU-C5/5-FU treated with LS-1 of 7.1 μM (IC50), we could observe the various apoptotic characteristics, such as the increase of apoptotic bodies, the increase of the sub-G1 hypodiploid cell population, the decrease of the Bcl-2 level, the increase of procaspase-9 cleavage, the increase of procaspase-3 cleavage and the increase of poly(ADP-ribose) polymerase cleavage. Interestingly, the apoptosis-induction effect of LS-1 was also accompanied by the increase of Smad-3 phosphorylation and the downregulation of c-Myc in SNU-C5/5-FU. LS-1 also increased the nuclear localization of phospho-Smad-3 and Smad-4. We examined whether LS-1 could downregulate the expression of carcinoembryonic antigen (CEA), a direct inhibitor of TGF-β signaling. LS-1 decreased the CEA level, as well as the direct interactio...Continue Reading

References

Dec 2, 1999·Journal of Natural Products·C Y DuhC F Dai
Mar 10, 2000·Cytokine & Growth Factor Reviews·S J KimY J Bang
Jun 28, 2000·Journal of Natural Products·C Y DuhC F Dai
Aug 22, 2001·Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Médicas E Biológicas·I GrivicichG Schwartsmann
Dec 12, 2001·Nature Cell Biology·Chuan-Wei JangRuey-Hwa Chen
Jul 13, 2006·The Journal of Cell Biology·Sylvie ThuaultAristidis Moustakas
Jan 24, 2007·Physiological Reviews·Karen Bedard, Karl-Heinz Krause
Sep 26, 2007·The Journal of Biological Chemistry·Min ChenJin Wang
Feb 22, 2008·CA: a Cancer Journal for Clinicians·Ahmedin JemalMichael J Thun
Oct 29, 2008·Oncogene·K W Yip, J C Reed
Apr 28, 2010·Archives of Pharmacal Research·Huu Tung NguyenYoung Ho Kim
Oct 16, 2012·Circulation Research·Lorenzo GalluzziGuido Kroemer
Feb 9, 2013·The Journal of Clinical Investigation·Neil E BholaCarlos L Arteaga
Jul 3, 2013·Drug Design, Development and Therapy·Hsin-chung LeeAkon Higuchi
Aug 16, 2013·Current Pharmaceutical Design·Isabel FabregatPatricia Sancho
Nov 19, 2013·Biomolecules & Therapeutics·Yhun Yhong SheenJeong-Seok Nam
Apr 5, 2014·Marine Drugs·Ahmed ElkhateebMohamed-Elamir F Hegazy

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Citations

Mar 16, 2017·Natural Product Reports·John W BluntMichèle R Prinsep
Nov 7, 2015·Marine Drugs·Sergey A Dyshlovoy, Friedemann Honecker

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Methods Mentioned

BETA
flow cytometry
confocal microscopy
immunoprecipitation
enzyme-linked immunosorbent assay
fluorescence-activated

Software Mentioned

Cell Quest

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