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整合素连接激酶与阿贝尔森激酶抑制对胶质母细胞瘤细胞异常有丝分裂和细胞死亡的联合作用

Combination Effects of Integrin-linked Kinase and Abelson Kinase Inhibition on Aberrant Mitosis and Cell Death in Glioblastoma Cells.

作者信息

Cunningham Abigail, Brown Maddisen, Dresselhuis Jonathan, Robinson Nicole, Hervie Keni, Cox Michael E, Mills Julia

机构信息

Department of Biology, Trinity Western University, Langley, BC V2Y 1Y1, Canada.

Vancouver Prostate Center and Vancouver Coastal Health Research Institute, Vancouver, BC V6T 1Z3, Canada.

出版信息

Biology (Basel). 2023 Jun 25;12(7):906. doi: 10.3390/biology12070906.

Abstract

In cancer cells, inhibition of integrin-linked kinase (ILK) increases centrosome declustering causing mitotic arrest and cell death. Yet, not all cancer cells are susceptible to anti-ILK treatment alone. We investigate a combination drug strategy targeting ILK and another oncogenic kinase, Abelson kinase (ABL). Drug-concentration viability assays (i.e., MTT assays) indicate that ILK and ABL inhibitors in combination decreased the viability of glioblastoma cells over the ILK drug QLT-0267 alone. Combination strategies also increased aberrant mitoses and cell death over QLT-0267 alone. This was evident from an increase in mitotic arrest, apoptosis and a sub-G1 peak following FAC analysis. In vitro, ILK and ABL localized to the centrosome and the putative ILK kinase domain was important for this localization. Increased levels of cytosolic ABL are associated with its transformative abilities. ILK inhibitor effects on survival correlated with its ability to decrease cytosolic ABL levels and inhibit ABL's localization to mitotic centrosomes in glioblastoma cells. ILK inhibitor effects on ABL's centrosomal localization were reversed by the proteasomal inhibitor MG132 (a drug that inhibits ABL degradation). These results indicate that ILK regulates ABL at mitotic centrosomes and that combination treatments targeting ILK and ABL are more effective then QLT-0267 alone at decreasing the survival of dividing glioblastoma cells.

摘要

在癌细胞中,抑制整合素连接激酶(ILK)会增加中心体解聚,导致有丝分裂停滞和细胞死亡。然而,并非所有癌细胞都单独对抗ILK治疗敏感。我们研究了一种针对ILK和另一种致癌激酶——阿贝尔森激酶(ABL)的联合用药策略。药物浓度活力测定(即MTT测定)表明,与单独使用ILK药物QLT-0267相比,ILK和ABL抑制剂联合使用降低了胶质母细胞瘤细胞的活力。联合用药策略还比单独使用QLT-0267增加了异常有丝分裂和细胞死亡。这从流式细胞术分析后有丝分裂停滞、凋亡增加以及亚G1峰中可以明显看出。在体外,ILK和ABL定位于中心体,推测的ILK激酶结构域对此定位很重要。胞质ABL水平升高与其转化能力相关。ILK抑制剂对存活的影响与其降低胶质母细胞瘤细胞胞质ABL水平以及抑制ABL定位于有丝分裂中心体的能力相关。蛋白酶体抑制剂MG132(一种抑制ABL降解的药物)可逆转ILK抑制剂对ABL中心体定位的影响。这些结果表明,ILK在有丝分裂中心体处调节ABL,并且针对ILK和ABL的联合治疗在降低分裂的胶质母细胞瘤细胞存活率方面比单独使用QLT-0267更有效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04af/10376030/2826a6d2df07/biology-12-00906-g001.jpg

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