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苄基异硫氰酸酯诱导肝癌细胞凋亡并抑制其迁移和侵袭

Benzyl-isothiocyanate Induces Apoptosis and Inhibits Migration and Invasion of Hepatocellular Carcinoma Cells .

作者信息

Zhu Mingyue, Li Wei, Dong Xu, Chen Yi, Lu Yan, Lin Bo, Guo Junli, Li Mengsen

机构信息

Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical College, Haikou 571199, Hainan Province, PR. China.; Key Laboratory of Molecular Biology, Hainan Medical College, Haikou 571199, Hainan Province, PR. China.

Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical College, Haikou 571199, Hainan Province, PR. China.

出版信息

J Cancer. 2017 Jan 15;8(2):240-248. doi: 10.7150/jca.16402. eCollection 2017.

DOI:10.7150/jca.16402
PMID:28243328
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5327373/
Abstract

Despite consideration of benzyl isothiocyanate(BITC) is applied to prevention and therapeutic of cancer, the role of BITC in inducing apoptosis, and inhibiting migration and invasion of hepatocellular carcinoma(HCC) cells is still unclear. In this study, we aim to explore the effects of BITC on the growth, migration and invasion of HCC cells in vitro. When human HCC cell lines, Bel 7402 and HLE, were treated with an optimal concentration of BITC for 48 hours, the results indicated that BITC inhibits growth and promotes apoptosis of HCC cells; BITC has a significant inhibitory effect on the migration and invasion of HCC cells. BITC stimulated expression of caspase-3/8 and PARP-1, and suppressed expression of survivin, MMP2/9 and CXCR4. BITC also inhibited the enzymatic activities of MMP2 and MMP9. Altogether, BITC was able to induce apoptosis and suppress the invasive and migratory abilities of Bel 7402 and HLE cells. The role mechanism of BITC might involve an up-regulating the expression of apoptosis-related proteins and down-regulating the expression of metastasis-related proteins. BITC may be applied as a novel chemotherapy for HCC patients.

摘要

尽管异硫氰酸苄酯（BITC）已被用于癌症的预防和治疗，但其在诱导肝癌（HCC）细胞凋亡以及抑制其迁移和侵袭方面的作用仍不清楚。在本研究中，我们旨在探讨BITC对体外培养的HCC细胞生长、迁移和侵袭的影响。当用人肝癌细胞系Bel 7402和HLE，以最佳浓度的BITC处理48小时后，结果表明BITC抑制HCC细胞的生长并促进其凋亡；BITC对HCC细胞的迁移和侵袭具有显著的抑制作用。BITC刺激caspase-3/8和PARP-1的表达，并抑制survivin、MMP2/9和CXCR4的表达。BITC还抑制MMP2和MMP9的酶活性。总之，BITC能够诱导Bel 7402和HLE细胞凋亡，并抑制其侵袭和迁移能力。BITC的作用机制可能涉及上调凋亡相关蛋白的表达和下调转移相关蛋白的表达。BITC可能作为一种新型的化疗药物应用于HCC患者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/273e204b956d/jcav08p0240g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/64454123fe2a/jcav08p0240g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/735918e76115/jcav08p0240g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/3cab860a7439/jcav08p0240g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/b5daa82cb6e0/jcav08p0240g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/273e204b956d/jcav08p0240g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/64454123fe2a/jcav08p0240g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/735918e76115/jcav08p0240g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/3cab860a7439/jcav08p0240g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/b5daa82cb6e0/jcav08p0240g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69e7/5327373/273e204b956d/jcav08p0240g005.jpg

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