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热休克蛋白90/蛋白激酶B信号通路可能介导蒿甲醚诱导的Cal27细胞凋亡。

The HSP90/Akt pathway may mediate artemether-induced apoptosis of Cal27 cells.

作者信息

Wu Jianhua, Li Lei, Wang Yiting, Ren Xiaobin, Lin Ken, He Yongwen

机构信息

Department of Periodontology, The Affiliated Stomatological Hospital of Kunming Medical University, Kunming, China.

Department of Head and Neck Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, China.

出版信息

FEBS Open Bio. 2019 Oct;9(10):1726-1733. doi: 10.1002/2211-5463.12711. Epub 2019 Aug 30.

DOI:10.1002/2211-5463.12711
PMID:31376209
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6768108/
Abstract

Tongue squamous cell carcinoma is the most common malignant tumor in oral and maxillofacial regions. Recent research has found that artemether can inhibit growth and induce apoptosis of cancer cells, although the mechanism is not clear. The present study aimed to explore the correlation between the HSP90/Akt pathway and artemether-induced apoptosis of Cal27 cells. A cell counting kit-8 and flow cytometry were used to detect the proliferation and apoptosis of Cal27 cells, respectively, mRNA expression was examined by quantitative RT-PCR, and protein expression was detected by western blotting. Our data revealed that artemether can inhibit growth and induce apoptosis of Cal27 cells. As the artemether concentration was increased, we observed downregulation of the expression of HSP90, p-Akt and p-mTOR in Cal27 cells, whereas the expression of Akt was not significantly changed. We also observed a time-dependent decrease in the expression of HSP90, p-Akt and p-mTOR during exposure to 0.1 mg·mL artemether. In conclusion, the HSP90/Akt pathway may be involved in artemether-induced apoptosis of Cal27 cells.

摘要

舌鳞状细胞癌是口腔颌面部最常见的恶性肿瘤。最近的研究发现,蒿甲醚可以抑制癌细胞的生长并诱导其凋亡,但其机制尚不清楚。本研究旨在探讨HSP90/Akt信号通路与蒿甲醚诱导的Cal27细胞凋亡之间的相关性。分别使用细胞计数试剂盒-8和流式细胞术检测Cal27细胞的增殖和凋亡情况,通过定量RT-PCR检测mRNA表达,通过蛋白质印迹法检测蛋白质表达。我们的数据显示,蒿甲醚可以抑制Cal27细胞的生长并诱导其凋亡。随着蒿甲醚浓度的增加,我们观察到Cal27细胞中HSP90、p-Akt和p-mTOR的表达下调,而Akt的表达没有明显变化。在暴露于0.1mg·mL蒿甲醚的过程中,我们还观察到HSP90、p-Akt和p-mTOR的表达呈时间依赖性下降。总之,HSP90/Akt信号通路可能参与了蒿甲醚诱导的Cal27细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a0/6768108/ad90c9b11c01/FEB4-9-1726-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a0/6768108/bb14a3f9c664/FEB4-9-1726-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a0/6768108/1e0b21ada4b6/FEB4-9-1726-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a0/6768108/ad90c9b11c01/FEB4-9-1726-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a0/6768108/bb14a3f9c664/FEB4-9-1726-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a0/6768108/1e0b21ada4b6/FEB4-9-1726-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a0/6768108/ad90c9b11c01/FEB4-9-1726-g003.jpg

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