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蜈蚣提取物诱导A375人黑色素瘤细胞的细胞周期停滞和凋亡。

Extracts of centipede induce cell cycle arrest and apoptosis in A375 human melanoma cells.

作者信息

Ma Weina, Liu Rui, Qi Junpeng, Zhang Yanmin

机构信息

School of Pharmacy, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.

出版信息

Oncol Lett. 2014 Jul;8(1):414-420. doi: 10.3892/ol.2014.2139. Epub 2014 May 12.

DOI:10.3892/ol.2014.2139
PMID:24959287
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4063562/
Abstract

Extracts from the centipede genus, have been used in traditional medicine for the treatment of various diseases and have been found to exhibit anticancer activity in tumor cells. To investigate the potential and associated antitumor mechanism of alcohol extracts of the centipede (AECS), cell viability, cell cycle and cell apoptosis were studied and the results revealed that AECS inhibits A375 cell proliferation in a dose- and time-dependent manner. In addition, AECS was found to arrest the cell cycle of A375 cells at the S phase, which was accompanied by a marked increase in the protein levels of cyclin E and a decrease in the protein levels of cyclin D1. In a cell culture system, AECS markedly induced the apoptosis of A375 cells, which was closely associated with the effects on the Bcl-2 family, whereby decreased Bcl-2 and increased Bak, Bax and Bad expression levels were observed. The underlying mechanism of AECS inhibiting A375 cell proliferation was associated with the induction of cell cycle arrest and apoptosis, indicating that AECS may present as a potential therapeutic agent for administration in human melanoma cancer intervention.

摘要

蜈蚣属提取物在传统医学中用于治疗各种疾病，并且已发现在肿瘤细胞中具有抗癌活性。为了研究蜈蚣醇提取物（AECS）的潜力及其相关的抗肿瘤机制，对细胞活力、细胞周期和细胞凋亡进行了研究，结果显示AECS以剂量和时间依赖性方式抑制A375细胞增殖。此外，发现AECS使A375细胞的细胞周期停滞于S期，同时伴随着细胞周期蛋白E蛋白水平的显著增加和细胞周期蛋白D1蛋白水平的降低。在细胞培养系统中，AECS显著诱导A375细胞凋亡，这与对Bcl-2家族的影响密切相关，由此观察到Bcl-2表达降低，Bak、Bax和Bad表达水平升高。AECS抑制A375细胞增殖的潜在机制与诱导细胞周期停滞和凋亡有关，表明AECS可能是一种用于人类黑色素瘤癌症干预的潜在治疗剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/c0711a1b0ab3/OL-08-01-0414-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/7fba07bd6830/OL-08-01-0414-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/4b9f4d7b197d/OL-08-01-0414-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/c0e39d3732af/OL-08-01-0414-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/3eba1ceb044b/OL-08-01-0414-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/f018c2e62b51/OL-08-01-0414-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/c0711a1b0ab3/OL-08-01-0414-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/7fba07bd6830/OL-08-01-0414-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/4b9f4d7b197d/OL-08-01-0414-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/c0e39d3732af/OL-08-01-0414-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/3eba1ceb044b/OL-08-01-0414-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/f018c2e62b51/OL-08-01-0414-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa4f/4063562/c0711a1b0ab3/OL-08-01-0414-g05.jpg

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