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白细胞介素-6 可刺激胰腺癌细胞系中的 STAT3 和 Pim-1 激酶。

IL-6 stimulates STAT3 and Pim-1 kinase in pancreatic cancer cell lines.

机构信息

College of Medicine, University of Arizona Cancer Center, Tucson, AZ 85724, USA.

出版信息

Pancreas. 2012 Jul;41(5):773-81. doi: 10.1097/MPA.0b013e31823cdd10.

DOI:10.1097/MPA.0b013e31823cdd10
PMID:22273698
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3337960/
Abstract

OBJECTIVES

We investigated the signaling pathways activated in response to interleukin 6 (IL-6) in pancreatic cell lines, with a focus on signal transducer and activator of transcription 3 (STAT3) and proto-oncogene serine/threonine-protein (Pim-1) kinase.

METHODS

Interleukin 6 receptor (IL-6R) expression and IL-6-induced cell signaling was measured by Western blotting in human pancreatic cell lines. Cucurbitacin I was used as a pharmacological tool to investigate the role of STAT3 in Pim-1 activation. Stably overexpressing Pim-1 kinase cell lines were characterized for their response to IL-6 in vitro and for their growth rate as flank tumors in scid mice.

RESULTS

Interleukin 6 receptor was expressed across multiple cancer cell lines. In Panc-1 cells, IL-6 treatment increased expression of phosphorylation of signal transducer and activator of transcription 3 and Pim-1 kinase. Cucurbitacin I treatment alone increased pErk1/2 expression in wild-type and Pim-1-overexpressing cell lines and resulted in exaggerated Pim-1 kinase protein levels in control and IL-6-stimulated cells, suggesting that up-regulation of Pim-1 may be partially STAT3 independent. Pim-1 overexpression did not significantly affect growth rate in vitro or in vivo in Panc-1 or MiaPaCa2 cell lines.

CONCLUSIONS

Interleukin 6 activates STAT3 and stimulates Pim-1 kinase in pancreatic cell line models. The regulation and consequence of Pim-1 expression seems to be highly context dependent.

摘要

目的

我们研究了白细胞介素 6（IL-6）在胰腺细胞系中激活的信号通路，重点关注信号转导和转录激活因子 3（STAT3）和原癌基因丝氨酸/苏氨酸蛋白激酶（Pim-1）。

方法

通过 Western blot 法检测人胰腺细胞系中白细胞介素 6 受体（IL-6R）的表达和 IL-6 诱导的细胞信号转导。使用葫芦素 I 作为药理工具来研究 STAT3 在 Pim-1 激活中的作用。通过稳定过表达 Pim-1 激酶的细胞系，研究其对体外 IL-6 的反应以及在 scid 小鼠中作为侧腹肿瘤的生长速度。

结果

IL-6R 在多种癌细胞系中表达。在 Panc-1 细胞中，IL-6 处理增加了信号转导和转录激活因子 3 和 Pim-1 激酶的磷酸化表达。葫芦素 I 处理本身增加了野生型和 Pim-1 过表达细胞系中 pErk1/2 的表达，并导致对照和 IL-6 刺激细胞中 Pim-1 激酶蛋白水平的夸大，表明 Pim-1 的上调可能部分独立于 STAT3。Pim-1 过表达在体外或 Panc-1 或 MiaPaCa2 细胞系中的体内均未显著影响生长速度。

结论

白细胞介素 6 在胰腺细胞系模型中激活 STAT3 并刺激 Pim-1 激酶。Pim-1 表达的调节和后果似乎高度依赖于上下文。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/53e7b7fbfda6/nihms338612f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/30c4d1339b99/nihms338612f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/9dde75d51888/nihms338612f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/a981eedefffc/nihms338612f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/ec1939500221/nihms338612f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/53e7b7fbfda6/nihms338612f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/30c4d1339b99/nihms338612f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/9dde75d51888/nihms338612f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/a981eedefffc/nihms338612f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/ec1939500221/nihms338612f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ba0/3337960/53e7b7fbfda6/nihms338612f5.jpg

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