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【Cancer research】趋化因子受体CXCR6 和其配体CXCL

The chemokine receptor CXCR6 and its ligand CXCL16 are expressed in carcinomas and inhibit proliferation
趋化因子受体CXCR6 和其配体CXCL16 在肿瘤中的表达并能抑制增殖

The chemokine receptor CXCR6 and its ligand CXCL16 are involved in inflammation. Thus far, they were known to be expressed mainly by T cells and macrophages, respectively. However, we detected both in all of 170 human primary mammary carcinomas and at similar levels in all 8 human mammary carcinoma cell lines tested by microarray analysis. Expression was confirmed by reverse transcription-PCR and for the cell lines also by fluorescence-activated cell sorting analysis. CXCR6 and CXCL16 were also detected in several mouse and human mammary, colon, and pancreatic carcinoma cell lines. CXCL16 is a transmembrane protein from which the soluble chemokine can be cleaved off. The transmembrane form is present on the surface of the carcinoma cells. Surprisingly, suppression of either CXCR6 or CXCL16 led to greatly enhanced proliferation in vitro as well as in vivo, indicating that their interaction inhibits proliferation. This notion was verified using inhibitory antibodies and by introduction of CXCL16 into a rare CXCL16-negative cell line. The effect was mediated by the G protein-coupled receptor CXCR6 because it was blocked by the G protein inhibitor pertussis toxin. In contrast, the soluble CXCL16 chemokine enhanced proliferation, and this was also mediated by CXCR6 but not via G protein. It is remarkable that both CXCR6 and CXCL16 are expressed by all mammary carcinomas because cells that lose either acquire a growth advantage and should be selected during tumor progression. This suggests an unknown important role in tumor formation. Proteases, possibly macrophage derived, might convert inhibitory transmembrane CXCL16 into the stimulatory chemokine. 谢谢了 本人已认领该文编译,48小时后若未提交译文,请其他战友自由认领。 The chemokine receptor CXCR6 and its ligand CXCL16 are expressed in carcinomas and inhibit proliferation
趋化因子受体CXCR6 和其配体CXCL16 在肿瘤中的表达并能抑制增殖

The chemokine receptor CXCR6 and its ligand CXCL16 are involved in inflammation.
趋化因子受体CXCR6 和其配体CXCL16 可参与炎症。Thus far, they were known to be expressed mainly by T cells and macrophages, respectively.
到目前为止,人们知道它们主要分别表达于T细胞和巨噬细胞。 However, we detected both in all of 170 human primary mammary carcinomas and at similar levels in all 8 human mammary carcinoma cell lines tested by microarray analysis.
然而,我们应用微阵列方法检测170例人原发性乳腺癌和所有8例人乳腺癌细胞系,结果发现它们均表达于这些肿瘤和细胞系中。
Expression was confirmed by reverse transcription-PCR and for the cell lines also by fluorescence-activated cell sorting analysis. 它们的表达被RT-PCR和荧光活化细胞分离技术进一步证实。
CXCR6 and CXCL16 were also detected in several mouse and human mammary, colon, and pancreatic carcinoma cell lines.
CXCR6和CXCL16也在一些鼠和人乳腺、结肠和胰腺癌细胞系中被检测。
CXCL16 is a transmembrane protein from which the soluble chemokine can be cleaved off.
CXCL16是一种来自于可溶的化学因子裂解的跨膜蛋白。
The transmembrane form is present on the surface of the carcinoma cells.
这种跨膜型存在于癌细胞的表面。
Surprisingly, suppression of either CXCR6 or CXCL16 led to greatly enhanced proliferation in vitro as well as in vivo, indicating that their interaction inhibits proliferation. This notion was verified using inhibitory antibodies and by introduction of CXCL16 into a rare CXCL16-negative cell line.
令人惊奇的是,体内外实验均显示抑制CXCR6或CXCL16可导致细胞增殖活性增强,提示它们与抑制细胞增殖有关。
The effect was mediated by the G protein-coupled receptor CXCR6 because it was blocked by the G protein inhibitor pertussis toxin.
这种作用是通过G蛋白偶联受体CXCR6来介导的,因为其可被G蛋白抑制剂百日咳毒素所阻断。
In contrast, the soluble CXCL16 chemokine enhanced proliferation, and this was also mediated by CXCR6 but not via G protein.
相反,可溶性CXCL16化学因子可增强细胞的增殖,这种作用也是通过CXCR6介导的,而不是G蛋白。
It is remarkable that both CXCR6 and CXCL16 are expressed by all mammary carcinomas because cells that lose either acquire a growth advantage and should be selected during tumor progression.
很明显,CXCR6和CXCL16在所有的乳腺癌细胞中表达,是因为这些细胞丧失了获得生长优势,在肿瘤的进展中接受了选择。This suggests an unknown important role in tumor formation. Proteases, possibly macrophage derived, might convert inhibitory transmembrane CXCL16 into the stimulatory chemokine
这些研究表明巨噬细胞来源的蛋白酶在肿瘤形成中发挥着一个未知的重要作用,可将抑制因子跨膜CXCL16转换为刺激性的化学因子。 趋化因子受体CXCR6 和其配体CXCL16 在肿瘤中的表达并能抑制增殖

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作者:admin@医学,生命科学    2010-11-19 17:11
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