Apicularen A Induces Cell Death through Fas Ligand Up-Regulation and Microtubule Disruption by Tubulin Down-Regulation in HM7 Human Colon Cancer Cells.

Apicularen A Induces Cell Death through Fas Ligand Up-Regulation and Microtubule Disruption by Tubulin Down-Regulation in HM7 Human Colon Cancer Cells. Research Abstract Details 

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Apicularen A Induces Cell Death through Fas Ligand Up-Regulation and Microtubule Disruption by Tubulin Down-Regulation in HM7 Human Colon Cancer Cells. Abstract Text:

Jong-Seok Kim,Young-Chul Lee,Ho-Tak Nam,Ge Li,Eun-Jin Yun,Kyoung-Sub Song,Kang-Sik Seo,Ji-Hoon Park,Jong-Woong Ahn,Okpyo Zee,Jong-Il Park,Wan-Hee Yoon,Kyu Lim,Byung-Doo Hwang,Jong-Seok Kim,Young-Chul Lee,Ho-Tak Nam,Ge Li,Eun-Jin Yun,Kyoung-Sub Song,Kang-Sik Seo,Ji-Hoon Park,Jong-Woong Ahn,Okpyo Zee,Jong-Il Park,Wan-Hee Yoon,Kyu Lim,Byung-Doo Hwang,Jong-Seok Kim,Young-Chul Lee,Ho-Tak Nam,Ge Li,Eun-Jin Yun,Kyoung-Sub Song,Kang-Sik Seo,Ji-Hoon Park,Jong-Woong Ahn,Okpyo Zee,Jong-Il Park,Wan-Hee Yoon,Kyu Lim,Byung-Doo Hwang,

PURPOSE: Apicularen A has been shown to cause growth inhibition and apoptosis in several cancer cell lines. However, the mechanisms of apicularen A-induced cell death and in vivo effects remain unclear. In this study, we investigated the molecular mechanisms of apicularen A-induced cell death in HM7 human colon cancer cells in vitro and anticancer activity in vivo. EXPERIMENTAL DESIGN: We tested cytotoxicity with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, apoptosis with DNA fragmentation assay, mitochondrial membrane potential, and cell cycle with fluorescence-activated cell sorting. Caspase activation was done by fluorometry. Alterations of microtubule structure, tubulin protein, and mRNA level were assessed by immunofluorescence, Western blot, and reverse transcription-PCR. In vivo studies were assessed using nude mice tumor cell growth in xenograft model and liver colonization assay. RESULTS: Apicularen A treatment of HM7 cells inhibited cell growth and this inhibition was partially rescued by z-VAD-fmk. Apicularen A caused accumulation of sub-G(1)-G(0), DNA fragmentation, Fas ligand induction, and activation of caspase-8 and caspase-3, but mitochondrial membrane potential was not changed. Furthermore, beta-tubulin protein and mRNA were decreased by apicularen A, but in vitro polymerization of tubulin was not affected. Concurrently, apicularen A-treated cell showed disruption of microtubule architecture. In in vivo studies, apicularen A reduced tumor volume by approximately 72% at the end of a 15-day treatment. Moreover, apicularen A reduced liver colonization as much as 95.6% (50 mug/kg/d). CONCLUSION: Apicularen A induces cell death of HM7 cells through up-regulating Fas ligand and disruption of microtubule architecture with down-regulation of tubulin level. These findings indicate that apicularen A is a promising new microtubule-targeting compound.

Apicularen A Induces Cell Death through Fas Ligand Up-Regulation and Microtubule Disruption by Tubulin Down-Regulation in HM7 Human Colon Cancer Cells. Publishing Authors By Initials

JS Kim,YC Lee,HT Nam,G Li,EJ Yun,KS Song,KS Seo,JH Park,JW Ahn,O Zee,JI Park,WH Yoon,K Lim,BD Hwang,JS Kim,YC Lee,HT Nam,G Li,EJ Yun,KS Song,KS Seo,JH Park,JW Ahn,O Zee,JI Park,WH Yoon,K Lim,BD Hwang,JS Kim,YC Lee,HT Nam,G Li,EJ Yun,KS Song,KS Seo,JH Park,JW Ahn,O Zee,JI Park,WH Yoon,K Lim,BD Hwang,

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Apicularen A Induces Cell Death through Fas Ligand Up-Regulation and Microtubule Disruption by Tubulin Down-Regulation in HM7 Human Colon Cancer Cells. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Clinical cancer research : an official journal of

VOLUME: 13

Page Numbers: 6509-17

Journal Abbreviation: Clin. Cancer Res.

ISSN: 1078-0432

DAY: 1

MONTH: Nov

YEAR: 2007

Apicularen A Induces Cell Death through Fas Ligand Up-Regulation and Microtubule Disruption by Tubulin Down-Regulation in HM7 Human Colon Cancer Cells. Information

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LANGUAGE: eng

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AFFILIATION: Authors' Affiliations: Department of Biochemistry, College of Medicine, Cancer Research Institute, and Research Institute for Medical Science, Chungnam National University, Daejeon, Republic of Korea.

Country: United States

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