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纳米二氨基四嗪增强吉非替尼对结直肠癌细胞的抗增殖作用：通过 EGFR 唾液酸化和 PI3K 激活介导。

Enhancement by Nano-Diamino-Tetrac of Antiproliferative Action of Gefitinib on Colorectal Cancer Cells: Mediation by EGFR Sialylation and PI3K Activation.

机构信息

Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, 11031, Taiwan.

Division of Colorectal Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, 23561, Taiwan.

出版信息

Horm Cancer. 2018 Dec;9(6):420-432. doi: 10.1007/s12672-018-0341-x. Epub 2018 Sep 5.

DOI:10.1007/s12672-018-0341-x
PMID:30187356
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6223990/
Abstract

Drug resistance complicates the clinical use of gefitinib. Tetraiodothyroacetic acid (tetrac) and nano-diamino-tetrac (NDAT) have been shown in vitro and in xenografts to have antiproliferative/angiogenic properties and to potentiate antiproliferative activity of other anticancer agents. In the current study, we investigated the effects of NDAT on the anticancer activities of gefitinib in human colorectal cancer cells. β-Galactoside α-2,6-sialyltransferase 1 (ST6Gal1) catalyzes EGFR sialylation that is associated with gefitinib resistance in colorectal cancers, and this was also investigated. Gefitinib inhibited cell proliferation of HT-29 cells (K-ras wild-type), and NDAT significantly enhanced the antiproliferative action of gefitinib. Gefitinib inhibited cell proliferation of HCT116 cells (K-ras mutant) only in high concentration, and this was further enhanced by NDAT. NDAT enhancedd gefitinib-induced antiproliferation in gefitinib-resistant colorectal cancer cells by inhibiting ST6Gal1 activity and PI3K activation. Furthermore, NDAT enhanced gefitinib-induced anticancer activity additively in colorectal cancer HCT116 cell xenograft-bearing nude mice. Results suggest that NDAT may have an application with gefitinib as combination colorectal cancer therapy.

摘要

耐药性使吉非替尼的临床应用变得复杂。四碘甲状腺原氨酸（tetrac）和纳米二氨基四（NDAT）已在体外和异种移植中显示出具有抗增殖/血管生成特性，并增强其他抗癌药物的抗增殖活性。在本研究中，我们研究了 NDAT 对人结直肠癌细胞中吉非替尼抗癌活性的影响。β-半乳糖苷α-2,6-唾液酸转移酶 1（ST6Gal1）催化 EGFR 唾液酸化，这与结直肠癌中的吉非替尼耐药性有关，我们也对此进行了研究。吉非替尼抑制 HT-29 细胞（K-ras 野生型）的细胞增殖，而 NDAT 显著增强了吉非替尼的抗增殖作用。吉非替尼仅在高浓度时抑制 HCT116 细胞（K-ras 突变型）的细胞增殖，而 NDAT 进一步增强了这种作用。NDAT 通过抑制 ST6Gal1 活性和 PI3K 激活，增强了吉非替尼耐药性结直肠癌细胞中吉非替尼诱导的增殖抑制作用。此外，NDAT 在结直肠癌细胞 HCT116 异种移植裸鼠中增强了吉非替尼诱导的抗癌活性。结果表明，NDAT 可能作为结直肠癌联合治疗与吉非替尼有应用前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/c801ef094a05/12672_2018_341_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/7c71dc207028/12672_2018_341_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/8e0065ee42a6/12672_2018_341_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/5c23b4296dba/12672_2018_341_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/230f3d8889ed/12672_2018_341_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/04412d9e6518/12672_2018_341_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/f5e362adc2b4/12672_2018_341_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/c801ef094a05/12672_2018_341_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/7c71dc207028/12672_2018_341_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/8e0065ee42a6/12672_2018_341_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/5c23b4296dba/12672_2018_341_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/230f3d8889ed/12672_2018_341_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/04412d9e6518/12672_2018_341_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/f5e362adc2b4/12672_2018_341_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9d2/10355904/c801ef094a05/12672_2018_341_Fig7_HTML.jpg

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