IL-6 signaling by STAT3 participates in the change from hyperplasia to neoplasia in NRP-152 and NRP-154 rat prostatic epithelial cells.
IL-6 signaling by STAT3 participates in the change from hyperplasia to neoplasia in NRP-152 and NRP-154 rat prostatic epithelial cells.
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DOI：
10.1186/1471-2407-1-19
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发表时间：
2001
期刊：
影响因子：
3.8
通讯作者：
Huang HF
中科院分区：
文献类型：
--
作者：
Barton BE;Murphy TF;Adem P;Watson RA;Irwin RJ;Huang HF
STAT3 磷酸化与多种癌症（包括前列腺癌）的肿瘤状态相关。我们研究了 2 只大鼠前列腺上皮细胞系中 IL-6 信号传导和 STAT3 磷酸化的作用。 NRP-152和NRP-154细胞源自同一大鼠前列腺，但NRP-152细胞不具有致瘤性，而NRP-154细胞具有致瘤性。这些线被认为代表前列腺癌发展的两个阶段：增生和瘤形成。信号通路的差异应该在两种表型（增生性和肿瘤性）中发挥作用。我们使用 STAT3 磷酸化特异性抗体，通过细胞内流式细胞术观察 STAT3 的磷酸化状态。我们使用相同的方法来检查细胞系产生的 IL-6。我们还通过荧光膜联蛋白 V 与细胞的结合来测量细胞凋亡。尽管两种细胞系都组成型产生IL-6，但未处理的NRP-154细胞中存在磷酸化-STAT3，但NRP-152细胞中不存在。地塞米松处理抑制了 NRP-152 细胞的 IL-6 产生，但增强了 NRP-154 细胞的 IL-6 产生。 JAK2 抑制剂 AG490 处理可诱导 NRP-152 细胞凋亡，但不会诱导 NRP-154 细胞凋亡。我们从这些实验中得出结论，STAT3 活性在 NRP-154 细胞的表型中起作用，但在 NRP-152 细胞的表型中不起作用。讨论了两种细胞系不同表型中替代 IL-6 信号传导途径的重要性。
STAT3 phosphorylation is associated with the neoplastic state in many types of cancer, including prostate cancer. We investigated the role of IL-6 signaling and phosphorylation of STAT3 in 2 rat prostatic epithelial lines. NRP-152 and NRP-154 cells were derived from the same rat prostate, yet the NRP-152 cells are not tumorigenic while the NRP-154 cells are tumorigenic. These lines are believed to represent 2 of the stages in the development of prostate cancer, hyperplasia and neoplasia. Differences in signaling pathways should play a role in the 2 phenotypes, hyperplastic and neoplastic. We looked at the phosphorylation state of STAT3 by intracellular flow cytometry, using phospho-specific antibodies to STAT3. We used the same method to examine IL-6 production by the cell lines. We also measured apoptosis by binding of fluorescent annexin V to the cells. Although both cells lines made IL-6 constitutively, phosphorylated-STAT3 was present in untreated NRP-154 cells, but not in NRP-152 cells. Treatment with dexamethasone inhibited the IL-6 production of NRP-152 cells, but enhanced that of NRP-154 cells. Treatment with the JAK2 inhibitor AG490 induced apoptosis in NRP-152, but not NRP-154 cells. We conclude from these experiments that STAT3 activity plays a role in the phenotype of NRP-154 cell, but not NRP-152 cells. The significance of alternative IL-6 signaling pathways in the different phenotypes of the 2 cell lines is discussed.
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影响因子：
20.3
作者：
BATAILLE, R;BARLOGIE, B;KLEIN, B
通讯作者：
KLEIN, B
影响因子：
20.3
作者：
Haddad, E;Paczesny, S;Fischer, A
通讯作者：
Fischer, A
影响因子：
--
作者：
HUANG, YW;VITETTA, ES
通讯作者：
VITETTA, ES
影响因子：
64.5
作者：
Bromberg, JF;Wrzeszczynska, MH;Darnell, JE
通讯作者：
Darnell, JE
影响因子：
4
作者：
Ihle, JN
通讯作者：
Ihle, JN