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MDA-19通过抑制PI3K/Akt信号通路抑制黑色素瘤进展。

MDA-19 Suppresses Progression of Melanoma Via Inhibiting the PI3K/Akt Pathway.

作者信息

Dang Ningning, Meng Xianguang, Ma Shanshan, Zhang Qian, Sun XiYa, Wei Jingjing, Huang Shuhong

机构信息

Department of Dermatology, Jinan Central Hospital affiliated to Shandong University, Jinan 250013, Shandong Province, P.R. China.

The First Clinical Medical College of Lanzhou University, Lanzhou 730000, Gansu Province, P.R. China.

出版信息

Open Med (Wars). 2018 Dec 16;13:416-424. doi: 10.1515/med-2018-0061. eCollection 2018.

DOI:10.1515/med-2018-0061
PMID:30613786
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6310917/
Abstract

OBJECTIVE

To investigate the effect of MDA-19 on progression of melanoma, and explore the relevant mechanism.

METHODS

The melanoma cell lines, M14 and UACC257, were treated with different concentrations of MDA-19, then CCK8, clone formation assay, Transwell and flow cytometry assays were performed to examine cell proliferation, migration, invasion and apoptosis, respectively. The expression of apoptosis-related proteins (Bcl-2, Bax and caspase 3 P17), EMT and signaling pathway-related proteins were also detected by Western blot.

RESULTS

MDA-19 inhibited melanoma cells in a dose-dependent manner. Compared to the NC group, MDA-19 significantly inhibited cell growth capacity, migration and invasion of M14 and UACC257 cells, and accelerated cell apoptosis in a mitochondrial pathway through regulating Bcl-2/Bax and Caspase 3 in M14 and UACC257 cells. Moreover, MDA-19 was observed to up-regulate the expression of E-cad and down-regulate the expression of N-cad, Vimentin and Slug in melanoma cells in vitro. Furthermore, MDA-19 could inhibit the PI3K/Akt pathway by blocking Akt phosphorylation (p-Akt) and downstream proteins, P70 and Cyclin D1 in M14 and UACC257 cells.

CONCLUSION

Our data demonstrate that MDA-19 could inhibit progression of melanoma by suppressing the PI3K/Akt pathway, suggesting that MDA-19 is a potential anti-cancer agent for therapy of melanoma.

摘要

目的

研究MDA - 19对黑色素瘤进展的影响，并探讨相关机制。

方法

用不同浓度的MDA - 19处理黑色素瘤细胞系M14和UACC257，然后分别进行CCK8、克隆形成试验、Transwell试验和流式细胞术检测，以检测细胞增殖、迁移、侵袭和凋亡情况。还通过蛋白质免疫印迹法检测凋亡相关蛋白（Bcl - 2、Bax和半胱天冬酶3 P17）、上皮 - 间质转化（EMT）和信号通路相关蛋白的表达。

结果

MDA - 19以剂量依赖性方式抑制黑色素瘤细胞。与阴性对照组相比，MDA - 19显著抑制M14和UACC257细胞的生长能力、迁移和侵袭，并通过调节M14和UACC257细胞中的Bcl - 2/Bax和半胱天冬酶3，在线粒体途径中加速细胞凋亡。此外，在体外观察到MDA - 19上调黑色素瘤细胞中E - cad的表达，下调N - cad、波形蛋白和锌指蛋白Slug的表达。此外，MDA - 19可通过阻断M14和UACC257细胞中Akt磷酸化（p - Akt）及其下游蛋白P70和细胞周期蛋白D1来抑制PI3K/Akt信号通路。

结论

我们的数据表明，MDA - 19可通过抑制PI3K/Akt信号通路来抑制黑色素瘤的进展，提示MDA - 19是一种治疗黑色素瘤的潜在抗癌药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/9cee91177524/med-13-416-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/ad7495661456/med-13-416-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/a9fb889eac38/med-13-416-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/eea8c6125d10/med-13-416-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/2e8c3ab50199/med-13-416-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/9cee91177524/med-13-416-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/ad7495661456/med-13-416-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/a9fb889eac38/med-13-416-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/eea8c6125d10/med-13-416-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/2e8c3ab50199/med-13-416-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f63a/6310917/9cee91177524/med-13-416-g005.jpg

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