CXCL17 expression by tumor cells recruits CD11b+Gr1 high F4/80- cells and promotes tumor progression.
CXCL17 expression by tumor cells recruits CD11b+Gr1 high F4/80- cells and promotes tumor progression.
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DOI：
10.1371/journal.pone.0044080
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Murakami T
中科院分区：
文献类型：
--
作者：
Matsui A;Yokoo H;Negishi Y;Endo-Takahashi Y;Chun NA;Kadouchi I;Suzuki R;Maruyama K;Aramaki Y;Semba K;Kobayashi E;Takahashi M;Murakami T
趋化因子参与肿瘤发生的发病机制和细胞运输的多个方面。在这项研究中，我们报告了C-X-C型趋化因子CXCL 17（DMC/VCC-1）的最新成员，招募未成熟的骨髓源性细胞并促进早期肿瘤进展。CXCL 17在某些侵袭性类型的胃肠道、乳腺和肺癌细胞中优先表达。CXCL 17表达在体外并未赋予NIH 3 T3细胞致癌潜力，但表达CXCL 17的NIH 3 T3细胞可在免疫缺陷小鼠中形成富含血管的肿瘤。我们的数据显示，表达CXCL 17的肿瘤细胞增加了小鼠肿瘤部位未成熟的CD 11b + Gr 1+髓源性细胞，并促进了CD 31+肿瘤血管生成。广泛的趋化性试验证明，CXCL 17应答细胞是CD 11b + Gr 1highF 4/80−细胞（约90%），在体外具有嗜中性粒细胞样形态。尽管CXCL 17表达不能增加荷瘤SCID小鼠中CD 11b + Gr 1+细胞的数量，也不能促进低转移性结肠癌细胞的转移，但CXCL 17反应性骨髓源性细胞的存在引起异种移植肿瘤形成的显著增强。这些结果表明，CXCL 17在肿瘤细胞中的异常表达招募未成熟的骨髓源性细胞，并通过血管生成促进肿瘤进展。
Chemokines are involved in multiple aspects of pathogenesis and cellular trafficking in tumorigenesis. In this study, we report that the latest member of the C-X-C-type chemokines, CXCL17 (DMC/VCC-1), recruits immature myeloid-derived cells and enhances early tumor progression. CXCL17 was preferentially expressed in some aggressive types of gastrointestinal, breast, and lung cancer cells. CXCL17 expression did not impart NIH3T3 cells with oncogenic potential in vitro, but CXCL17-expressing NIH3T3 cells could form vasculature-rich tumors in immunodeficient mice. Our data showed that CXCL17-expressing tumor cells increased immature CD11b+Gr1+ myeloid-derived cells at tumor sites in mice and promoted CD31+ tumor angiogenesis. Extensive chemotactic assays proved that CXCL17-responding cells were CD11b+Gr1highF4/80− cells (∼90%) with a neutrophil-like morphology in vitro. Although CXCL17 expression could not increase the number of CD11b+Gr1+ cells in tumor-burdened SCID mice or promote metastases of low metastatic colon cancer cells, the existence of CXCL17-responding myeloid-derived cells caused a striking enhancement of xenograft tumor formation. These results suggest that aberrant expression of CXCL17 in tumor cells recruits immature myeloid-derived cells and promotes tumor progression through angiogenesis.
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影响因子：
11.2
作者：
Fridlender ZG;Buchlis G;Kapoor V;Cheng G;Sun J;Singhal S;Crisanti MC;Wang LC;Heitjan D;Snyder LA;Albelda SM
通讯作者：
Albelda SM
影响因子：
64.5
作者：
COPELAND, NG;COOPER, GM
通讯作者：
COOPER, GM
影响因子：
64.8
作者：
FUJITA, J;YOSHIDA, O;AARONSON, SA
通讯作者：
AARONSON, SA
影响因子：
6.5
作者：
Murakami, Takashi;Sato, Atsuko;Kobayashi, Eiji
通讯作者：
Kobayashi, Eiji
影响因子：
4.8
作者：
Holmqvist, K;Cross, MJ;Welsh, M
通讯作者：
Welsh, M