Epigenetic inactivation of protein kinase D1 in gastric cancer and its role in gastric cancer cell migration and invasion
Identifieur interne : 001334 ( Main/Exploration ); précédent : 001333; suivant : 001335Epigenetic inactivation of protein kinase D1 in gastric cancer and its role in gastric cancer cell migration and invasion
Auteurs : Mirang Kim [Corée du Sud] ; Hay-Ran Jang [Corée du Sud] ; Jeong-Hwan Kim [Corée du Sud] ; Seung-Moo Noh ; Kyu-Sang Song ; June-Sik Cho ; Hyun-Yong Jeong [Corée du Sud] ; Jim C. Norman [Royaume-Uni] ; Patrick T. Caswell [Royaume-Uni] ; Gyeong Hoon Kang [Corée du Sud] ; Seon-Young Kim [Corée du Sud] ; Hyang-Sook Yoo [Corée du Sud] ; Yong Sung Kim [Corée du Sud]Source :
- Carcinogenesis [ 0143-3334 ] ; 2008-02-17.
Abstract
Protein kinase D (PKD) 1 influences cell migration by mediating both trans-Golgi vesicle fission and integrin recycling to the cell surface. Using restriction landmark genomic scanning methods, we found that the promoter region of PKD1 was aberrantly methylated in gastric cancer cell lines. Silencing of PKD1 expression was detected in 72.7% of gastric cancer cell lines examined, and the silencing was associated with CpG hypermethylation in the promoter region of PKD1. Treatment with 5-aza-2-deoxycytidine and trichostatin A partially reversed PKD1 methylation and restored gene expression in PKD1-silenced cell lines. Real-time reverse transcriptionpolymerase chain reaction analysis of 96 paired clinical primary gastric cancer samples revealed that 59% of the analyzed tumors had a >2-fold decrease in PKD1 expression compared with each normal-appearing tissue and that this downregulation of PKD1 expression was significantly correlated with increased methylation. We also observed a gradual increase in the level of promoter methylation of PKD1 in aging, normal-appearing mucosal tissues, suggesting that PKD1 methylation may be one of the earliest events that predispose an individual to gastric cancer. PKD1 expression was required for directional migration of gastric cancer cells. Furthermore, knock down of PKD1 by RNA interference promoted the invasiveness of cell lines that expressed PKD1 at relatively high levels. Based on these results, we propose that PKD1 is frequently silenced by epigenetic regulation, which plays a role in cell migration and metastasis in gastric cancer.
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DOI: 10.1093/carcin/bgm291
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Norman</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Integrin Cell Biology Laboratory, Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD</wicri:regionArea><wicri:noRegion>Glasgow G61 1BD</wicri:noRegion></affiliation></author><author><name sortKey="Caswell, Patrick T" sort="Caswell, Patrick T" uniqKey="Caswell P" first="Patrick T." last="Caswell">Patrick T. 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Using restriction landmark genomic scanning methods, we found that the promoter region of PKD1 was aberrantly methylated in gastric cancer cell lines. Silencing of PKD1 expression was detected in 72.7% of gastric cancer cell lines examined, and the silencing was associated with CpG hypermethylation in the promoter region of PKD1. Treatment with 5-aza-2-deoxycytidine and trichostatin A partially reversed PKD1 methylation and restored gene expression in PKD1-silenced cell lines. Real-time reverse transcriptionpolymerase chain reaction analysis of 96 paired clinical primary gastric cancer samples revealed that 59% of the analyzed tumors had a >2-fold decrease in PKD1 expression compared with each normal-appearing tissue and that this downregulation of PKD1 expression was significantly correlated with increased methylation. We also observed a gradual increase in the level of promoter methylation of PKD1 in aging, normal-appearing mucosal tissues, suggesting that PKD1 methylation may be one of the earliest events that predispose an individual to gastric cancer. PKD1 expression was required for directional migration of gastric cancer cells. Furthermore, knock down of PKD1 by RNA interference promoted the invasiveness of cell lines that expressed PKD1 at relatively high levels. Based on these results, we propose that PKD1 is frequently silenced by epigenetic regulation, which plays a role in cell migration and metastasis in gastric cancer.</div></front></TEI><affiliations><list><country><li>Corée du Sud</li><li>Royaume-Uni</li></country><settlement><li>Séoul</li></settlement></list><tree><noCountry><name sortKey="Cho, June Sik" sort="Cho, June Sik" uniqKey="Cho J" first="June-Sik" last="Cho">June-Sik Cho</name><name sortKey="Noh, Seung Moo" sort="Noh, Seung Moo" uniqKey="Noh S" first="Seung-Moo" last="Noh">Seung-Moo Noh</name><name sortKey="Song, Kyu Sang" sort="Song, Kyu Sang" uniqKey="Song K" first="Kyu-Sang" last="Song">Kyu-Sang Song</name></noCountry><country name="Corée du Sud"><noRegion><name sortKey="Kim, Mirang" sort="Kim, Mirang" uniqKey="Kim M" first="Mirang" last="Kim">Mirang Kim</name></noRegion><name sortKey="Jang, Hay Ran" sort="Jang, Hay Ran" uniqKey="Jang H" first="Hay-Ran" last="Jang">Hay-Ran Jang</name><name sortKey="Jeong, Hyun Yong" sort="Jeong, Hyun Yong" uniqKey="Jeong H" first="Hyun-Yong" last="Jeong">Hyun-Yong Jeong</name><name sortKey="Kang, Gyeong Hoon" sort="Kang, Gyeong Hoon" uniqKey="Kang G" first="Gyeong Hoon" last="Kang">Gyeong Hoon Kang</name><name sortKey="Kim, Jeong Hwan" sort="Kim, Jeong Hwan" uniqKey="Kim J" first="Jeong-Hwan" last="Kim">Jeong-Hwan Kim</name><name sortKey="Kim, Mirang" sort="Kim, Mirang" uniqKey="Kim M" first="Mirang" last="Kim">Mirang Kim</name><name sortKey="Kim, Seon Young" sort="Kim, Seon Young" uniqKey="Kim S" first="Seon-Young" last="Kim">Seon-Young Kim</name><name sortKey="Kim, Yong Sung" sort="Kim, Yong Sung" uniqKey="Kim Y" first="Yong Sung" last="Kim">Yong Sung Kim</name><name sortKey="Kim, Yong Sung" sort="Kim, Yong Sung" uniqKey="Kim Y" first="Yong Sung" last="Kim">Yong Sung Kim</name><name sortKey="Kim, Yong Sung" sort="Kim, Yong Sung" uniqKey="Kim Y" first="Yong Sung" last="Kim">Yong Sung Kim</name><name sortKey="Yoo, Hyang Sook" sort="Yoo, Hyang Sook" uniqKey="Yoo H" first="Hyang-Sook" last="Yoo">Hyang-Sook Yoo</name></country><country name="Royaume-Uni"><noRegion><name sortKey="Norman, Jim C" sort="Norman, Jim C" uniqKey="Norman J" first="Jim C." last="Norman">Jim C. Norman</name></noRegion><name sortKey="Caswell, Patrick T" sort="Caswell, Patrick T" uniqKey="Caswell P" first="Patrick T." last="Caswell">Patrick T. Caswell</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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