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细胞周期蛋白依赖性激酶抑制剂（p16(INK4A)、p18(INK4C)、p19(INK4D)、p21(WAF1/CIP1) 和 p27(KIP1)）对恶性胶质瘤细胞的抗肿瘤作用。

Antitumour effect of cyclin-dependent kinase inhibitors (p16(INK4A), p18(INK4C), p19(INK4D), p21(WAF1/CIP1) and p27(KIP1)) on malignant glioma cells.

作者信息

Komata T, Kanzawa T, Takeuchi H, Germano I M, Schreiber M, Kondo Y, Kondo S

机构信息

Department of Neurosurgery, Mount Sinai School of Medicine, New York, NY 10029, USA.

出版信息

Br J Cancer. 2003 Apr 22;88(8):1277-80. doi: 10.1038/sj.bjc.6600862.

DOI:10.1038/sj.bjc.6600862
PMID:12698196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2747579/
Abstract

Cyclin-dependent kinase inhibitors (CDKIs) are considered as novel anticancer agents because of their ability to induce growth arrest or apoptosis in tumour cells. It has not yet been fully determined, however, which CDKI is the best candidate for the treatment of malignant gliomas and whether normal brain tissues are affected by CDKI expression. Using recombinant adenoviral vectors that express CDKIs (p16(INK4A), p18(INK4C), p19(INK4D), p21(WAF1/CIP1) and p27(KIP1)), we compared the antitumour effect of CDKIs on malignant glioma cell lines (A172, GB-1, T98G, U87-MG, U251-MG and U373-MG). p27(KIP1) showed higher ability to suppress the growth of all tumour cells tested than other CDKIs. Interestingly, overexpression of p27(KIP1) induced autophagic cell death, but not apoptosis in tumour cells. On the other hand, p27(KIP1) overexpression did not inhibit the viability of cultured astrocytes (RNB) nor induced autophagy. Overall, our findings suggest that gene transfer of p27(KIP1) may be a promising approach for the therapy of malignant gliomas.

摘要

细胞周期蛋白依赖性激酶抑制剂（CDKIs）因其能够诱导肿瘤细胞生长停滞或凋亡而被视为新型抗癌药物。然而，尚未完全确定哪种CDKI是治疗恶性胶质瘤的最佳候选药物，以及正常脑组织是否会受到CDKI表达的影响。我们使用表达CDKIs（p16(INK4A)、p18(INK4C)、p19(INK4D)、p21(WAF1/CIP1)和p27(KIP1)）的重组腺病毒载体，比较了CDKIs对恶性胶质瘤细胞系（A172、GB-1、T98G、U87-MG、U251-MG和U373-MG）的抗肿瘤作用。与其他CDKIs相比，p27(KIP1)对所有测试肿瘤细胞的生长抑制能力更强。有趣的是，p27(KIP1)的过表达诱导肿瘤细胞发生自噬性细胞死亡，而非凋亡。另一方面，p27(KIP1)的过表达并未抑制培养的星形胶质细胞（RNB）的活力，也未诱导自噬。总体而言，我们的研究结果表明，p27(KIP1)的基因转移可能是治疗恶性胶质瘤的一种有前景的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45fa/2747579/bb3373e0a4df/88-6600862f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45fa/2747579/eac9403435df/88-6600862f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45fa/2747579/e83c752e92a8/88-6600862f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45fa/2747579/bb3373e0a4df/88-6600862f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45fa/2747579/eac9403435df/88-6600862f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45fa/2747579/e83c752e92a8/88-6600862f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45fa/2747579/bb3373e0a4df/88-6600862f3.jpg

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