Resveratrol Inhibits Oesophageal Adenocarcinoma Cell Proliferation via AMP-activated Protein Kinase Signaling

Fan, Guang-Hua; Wang, Zhong-Ming; Yang, Xi; Xu, Li-Ping; Qin, Qin; Zhang, Chi; Ma, Jian-Xin; Cheng, Hong-Yan; Sun, Xin-Chen

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자료유형: 학술저널

저자정보: Fan, Guang-Hua (Department of Radiation Oncology, the First Affiliated Hospital of Nanjing Medical University) Wang, Zhong-Ming (Department of Radiation Oncology, the First Affiliated Hospital of Nanjing Medical University) Yang, Xi (Department of Radiation Oncology, the First Affiliated Hospital of Nanjing Medical University) Xu, Li-Ping (Department of Radiation Oncology, the First Affiliated Hospital of Nanjing Medical University) Qin, Qin (Department of Radiation Oncology, the First Affiliated Hospital of Nanjing Medical University) Zhang, Chi (Department of Radiation Oncology, the First Affiliated Hospital of Nanjing Medical University) Ma, Jian-Xin (Department of Radiation oncology, Lianyungang Second People's Hospital) Cheng, Hong-Yan (Department of Synthetic Internal Medicine, the First Affiliated Hospital of Nanjing Medical University) Sun, Xin-Chen (Department of Radiation Oncology, the First Affiliated Hospital of Nanjing Medical University)

저널정보: 아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제2호

발행연도: 2014.1

수록면: 677 - 682 (6page)

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Resveratrol has been examined in several model systems for potential effects against cancer. Adenosine monophosphate-activated protein kinase (AMPK) is reported to suppress proliferation in most eukaryocyte cells. Whether resveratrol via AMPK inhibits proliferation of oesophageal adenocarcinoma cells (OAC) is unknown. The aim of this study was to determine the roles of AMPK in the protective effects of resveratrol in OAC proliferation and to elucidate the underlying mechanisms. Treatment of cultured OAC derived from human subjects or cell lines with resveratrol resulted in decreased cell proliferation. Further, inhibition of AMPK by pharmacological reagent or genetical approach abolished resveratrol-suppressed OAC proliferation, reduced the level of $p27^{Kip1}$, a cyclin-dependent kinase inhibitor, and increased the levels of S-phase kinase-associated protein 2 (Skp2) of $p27^{Kip1}$-E3 ubiquitin ligase and 26S proteasome activity reduced by resveratrol. Furthermore, gene silencing of $p27^{Kip1}$ reversed resveratrol-suppressed OAC proliferation. In conclusion, these findings indicate that resveratrol inhibits Skp2-mediated ubiquitylation and 26S proteasome-dependent degradation of $p27^{Kip1}$ via AMPK activation to suppress OAC proliferation.

#AMPK #resveratrol #oesophageal adenocarcinoma #$p27^{Kip1}$ #proliferation

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Fan, Guang-Hua

소속기관 Department of Radiation Oncology, the First Affiliated Hospital of Nanjing Medical University