CXCL13 mediates prostate cancer cell proliferation through JNK signalling and invasion through ERK activation.
CXCL13 mediates prostate cancer cell proliferation through JNK signalling and invasion through ERK activation.
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DOI：
10.1111/j.1365-2184.2011.00757.x
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发表时间：
2011-08
影响因子：
8.5
通讯作者：
Lillard JW Jr
中科院分区：
文献类型：
--
作者：
El-Haibi CP;Singh R;Sharma PK;Singh S;Lillard JW Jr
本研究的重点是确定胞质分裂贡献因子2（DOCK 2）、细胞外信号调节激酶1/2（ERK 1/2）、c-Jun N末端激酶1（JNK）和Akt信号参与CXCL 13介导的前列腺癌（PCa）细胞侵袭和增殖。使用雄激素敏感（LNCaP）、雄激素难治性（PC 3）细胞和正常细胞（RWPE-1）来测定CXCL 13介导的PCa细胞侵袭和增殖。进行免疫印迹、基于快速活化细胞（FACE）的ELISA、半胱天冬酶活性、细胞侵袭和增殖测定以确定参与PCa细胞增殖和侵袭的一些信号传导事件。与雄激素敏感的LNCaP细胞不同，我们首次报道了耐药细胞系PC 3表达DOCK 2。CXCL 13介导的LNCaP和PC 3细胞侵袭受Akt和ERK 1/2激活的调节，其方式不依赖于DOCK 2。CXCL 13还以JNK依赖性方式促进LNCaP细胞增殖，即使在不存在DOCK 2的情况下。相反，CXCL 13通过JNK激活诱导PC 3细胞增殖，这需要DOCK 2。我们的研究结果表明CXCL 13介导的PCa细胞侵袭需要Akt和ERK 1/2激活，并表明DOCK 2在难治性CXCR 5阳性PCa细胞增殖中的新作用。
The focus of this study was to determine the dedicator of cytokinesis 2 (DOCK2), extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase-1 (JNK) and Akt signals involved in CXCL13-mediated prostate cancer (PCa) cell invasion and proliferation. Androgen-sensitive (LNCaP), hormone-refractory (PC3) cells and normal cells (RWPE-1) were used to determine CXCL13-mediated PCa cell invasion and proliferation. Immuno-blotting, fast activated cell-based (FACE) ELISA, caspase activity, cell invasion and proliferation assays were performed to ascertain some of the signalling events involved in PCa cell proliferation and invasion. Unlike androgen-sensitive LNCaP cells, we report for the first time that the hormone-refractory cell line, PC3, expresses DOCK2. CXCL13-mediated LNCaP and PC3 cell invasion was regulated by Akt and ERK1/2 activation in a DOCK2-independent fashion. CXCL13 also promoted LNCaP cell proliferation in a JNK-dependent fashion even in the absence of DOCK2. In contrast, CXCL13 induced PC3 cell proliferation through JNK activation, which required DOCK2. Our results show CXCL13-mediated PCa cell invasion requires Akt and ERK1/2 activation and suggests a new role for DOCK2 in proliferation of hormone-refractory CXCR5-positive PCa cells.
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发表时间：
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影响因子：
11.1
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