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IJC:卵巢癌细胞修改蛋白质CXCL10抑制机体免疫攻击

  1. CXCL10
  2. 免疫
  3. 卵巢癌

来源:生物谷 2013-09-28 06:59

2013年9月28日讯 /生物谷BIOON/--近日,科学家们发现癌症中与炎症相关的某一过程可能会导致拓宽某些类型卵巢肿瘤的治疗方案。 在Prince Henry研究所博士Andrew Stephens与Hasanuddin大学Monash Health的带领下,团队已经公布调查结果在International Journal of Cancer期刊上...

2013年9月28日讯 /生物谷BIOON/--近日,科学家们发现癌症中与炎症相关的某一过程可能会导致拓宽某些类型卵巢肿瘤的治疗方案。

在Prince Henry研究所博士Andrew Stephens与Hasanuddin大学Monash Health的带领下,团队已经公布调查结果在International Journal of Cancer期刊上,一些高等级的浆液性卵巢肿瘤修改一种蛋白质CXCL10,抑制免疫攻击。

卵巢癌生物标志物实验室主管Stephens博士说:在正常情况下,CXCL10鼓励白血细胞攻击肿瘤组织,但我们发现,某些卵巢肿瘤是可以修改CXCL10以防止这种情况发生。

这项研究提供了一种解释,某些卵巢肿瘤是如何阻断身体早期的抗肿瘤免疫反应,促进肿瘤的生长和转移。

众所周知,免疫与癌症进展有密切关联。这项研究增加了对某些肿瘤如何克服机体的抗肿瘤免疫反应,并有可能促进其扩散到身体其他部位的了解。

这一发现可能导致治疗某些类型的卵巢肿瘤出现一种新方法,团队现在正在试验针对这种肿瘤特定修改CXCL10的疗法, Stephens博士认为这可能对妇女肿瘤诊断有重大利益。

研究的下一个目标是,确定这种方法是否可以补充现有的治疗方法。通过提高免疫识别和破坏肿瘤细胞,研究者认为联合疗法可能会显著改善患者的治疗结果。(生物谷Bioon.com)

The role of melanoma tumor-derived nitric oxide in the tumor inflammatory microenvironment: Its impact on the chemokine expression profile, including suppression of CXCL10

Keiji Tanese,et al.

Melanoma appears to be heterogeneous in terms of its molecular biology, etiology and epidemiology. We previously reported that the expression of inducible nitric-oxide synthase (iNOS) in melanoma tumor cells is strongly correlated with poor patient survival. Therefore, we hypothesized that nitric oxide (NO) produced by iNOS promotes the melanoma inflammatory tumor microenvironment associated with poor outcome. To understand the role of NO and iNOS in the melanoma inflammatory tumor microenvironment, polymerase chain reaction arrays of inflammatory and autoimmunity genes were performed on a series of stage III melanoma lymph node metastasis samples to compare the gene expression profiles of iNOS-expressing and nonexpressing tumor samples. The results indicate that expression of CXC chemokine ligand 10 (CXCL10) was inversely correlated with iNOS expression, and the high CXCL10-expressing cases had more favorable prognoses than the low CXCL10-expressing cases. Functional studies revealed that treating iNOS-negative/CXCL10-positive melanoma cell lines with a NO donor suppressed the expression of CXCL10. Furthermore, scavenging NO from iNOS-expressing cell lines significantly affected the chemokine expression profile. Culture supernatants from NO scavenger-treated melanoma cells promoted the migration of plasmacytoid dendritic cells, which was diminished when the cells were treated with a CXCL10-neutralizing antibody. CXCL10 has been reported to be an antitumorigenic chemokine. Our study suggests that the production of NO by iNOS inhibits the expression of CXCL10 in melanoma cells and leads to a protumorigenic tumor microenvironment. Inhibiting NO induces an antitumorigenic environment, and thus, iNOS should be considered to be an important therapeutic target in melanoma.

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