Natriuretic peptide receptor A inhibition suppresses gastric cancer development through reactive oxygen species-mediated G2/M cell cycle arrest and cell death
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- 作者：Zheng Lia ; 1 ; Ji-Wei Wanga ; 1 ; Wei-Zhi Wanga ; 1 ; Xiao-Fei Zhia ; b ; 1 ; Qun Zhanga ; Bo-Wen Lia ; Lin-Jun Wanga ; Kun-Ling Xiea ; Jin-Qiu Taoa ; Jie Tanga ; Song Weia ; Yi Zhua ; Hao Xua ; Dian-Cai Zhanga ; Li Yanga ; Ze-Kuan Xua ; c ; xuzekuan@njmu.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：NPRA ; natriuretic peptide receptor A ; ANP ; atrial natriuretic peptide ; AMPK ; AMP-activated protein kinase ; ATG ; autophagy-related genes ; TMA ; tissue microarray assay ; ROS ; reactive oxygen species ; JNK ; c-Jun N-terminal kinase ; MAPKs ; mitogen-activated protein kinases ; DHE ; Dihydroethidium ; CCK-8 ; cell counting kit 8 ; 3-MA ; 3-methyladenine ; CQ ; chloroquine ; SEM ; standard error of the mean ; Z-VAD-FMK ; N-benzyloxycarbonyl-Val-Ala-Asp(O-Me) fluoromethyl ketone ; IRS ; immunoreactive score ; TUNEL ; term
- 刊名：Free Radical Biology and Medicine
- 出版年：2016
- 出版时间：October 2016
- 年：2016
- 卷：99
- 期：Complete
- 页码：593-607
- 全文大小：13285 K
文摘
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Higher NPRA expression indicates more advanced stage in gastric cancer.
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NPRA knockdown induces proliferation impairment and cell death in gastric cancer.
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ROS accumulates after NPRA knockdown and kills the gastric cancer cells.
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NPRA knockdown induces ROS-dependent cell protective autophagy.
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ROS activates JNK and AMPK after NPRA inhibition.