Pyk2 和 Src 介导 CCL18 诱导的乳腺癌转移信号。
Pyk2 and Src mediate signaling to CCL18-induced breast cancer metastasis.
机构信息
Breast Cancer Center, Sun-Yat-Sen Memorial Hospital, Sun-Yat-Sen University, Guangzhou, 510120, People's Republic of China; Department of Breast and Thyroid Surgery, The 6th Affriciated Hospital of Sun Yat-Sen University, Sun-Yat-Sen University, Guangzhou, 510120, People's Republic of China.
出版信息
J Cell Biochem. 2014 Mar;115(3):596-603. doi: 10.1002/jcb.24697.
Pyk2 and Src phosphorylation is initiated by CCL18, which promotes breast cancer metastasis via its functional G protein-coupled receptor PITPNM3. However, the function of Pyk2 and Src in CCL18-induced breast cancer metastasis is poorly understood. Quantitative reverse-transcription polymerase chain reactions (qRT-PCRs), Western blot, boyden chamber assay, and adherence assay were performed to delineate the consequences of Pyk2/Src in CCL18-induced breast cancer cells. Co-immunoprecipitation and immunofluorescence were performed to analyze the interaction of proteins. Upon the binding of CCL18 to PITPNM3, Pyk2 translocates from the cytoplasm to the plasma membrane to form a stable complex with PITPNM3, subsequently activating Src kinase. Moreover, upon stimulation with CCL18, Pyk2 and Src become essential for integrin alpha5/beta1 clustering-dependent adherence, migration, and invasion. Pyk2 and Src are important in CCL18-induced breast cancer metastasis.
CCL18 通过其功能性 G 蛋白偶联受体 PITPNM3 促进乳腺癌转移，其可引发 Pyk2 和 Src 的磷酸化。然而，CCL18 诱导的乳腺癌转移中 Pyk2 和 Src 的功能仍知之甚少。我们通过定量逆转录聚合酶链反应（qRT-PCR）、Western blot、Boyden 室测定和黏附测定来阐明 Pyk2/Src 在 CCL18 诱导的乳腺癌细胞中的作用。我们通过免疫共沉淀和免疫荧光分析来分析蛋白质的相互作用。当 CCL18 与 PITPNM3 结合时，Pyk2 从细胞质易位到质膜，与 PITPNM3 形成稳定的复合物，随后激活 Src 激酶。此外，在 CCL18 的刺激下，Pyk2 和 Src 对于整合素 α5/β1 聚类依赖性黏附、迁移和侵袭是必需的。Pyk2 和 Src 在 CCL18 诱导的乳腺癌转移中很重要。
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