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白细胞介素-8 和白细胞介素-17 与癌症。

Interleukin-8 and interleukin-17 for cancer.

机构信息

Department of Pulmonary, Oncology Unit, "G. Papanikolaou" General Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece;

出版信息

Cancer Invest. 2014 Jun;32(5):197-205. doi: 10.3109/07357907.2014.898156. Epub 2014 Mar 26.

Abstract

Pro-inflammatory cytokines have been associated with chronic inflammation and inflammatory diseases. Increased levels of interleukins (ILs) have been associated with inflammatory disease exacerbation. ILs levels have been observed to be associated with advance stage cancer for several types of cancer and a poor prognostic maker for malignant disease. Moreover; increased levels of cytokines induce tumorigenesis. There are several paradigms such as the hepatocellular carcinoma induced from chronic inflammation of an underlying hepatitis. In the current review, we will focus on IL-8 and -17. These two ILs as in the case of others, induce neo-angiogenesis through activation of the vascular endothelial growth (VEGF) factor pathway. Additionally, they enhance the activity of matrix metalloproteinase-2 and -9 (MMP-2,-9) which in turn increase the metastatic activity of the underlying malignancy. Inhibition of cytokine production could be a potential treatment both for chronic inflammatory diseases and tumor modulation. Local microenvironment modulation could be applied in surgery resected patients as in the case of lung cancer in order to enhance the local immune activity.

摘要

促炎细胞因子与慢性炎症和炎症性疾病有关。白细胞介素(ILs)水平升高与炎症性疾病恶化有关。已经观察到几种类型癌症的癌症晚期和恶性疾病预后不良与 ILs 水平有关。此外,细胞因子水平升高可诱导肿瘤发生。有几种范例,例如由潜在肝炎的慢性炎症引起的肝细胞癌。在当前的综述中,我们将重点关注 IL-8 和 -17。这两种 IL 与其他 IL 一样,通过激活血管内皮生长(VEGF)因子途径诱导新血管生成。此外,它们增强基质金属蛋白酶-2 和 -9(MMP-2,-9)的活性,从而增加潜在恶性肿瘤的转移活性。抑制细胞因子的产生可能是治疗慢性炎症性疾病和肿瘤调节的一种潜在方法。局部微环境调节可应用于手术切除的患者,如肺癌患者,以增强局部免疫活性。

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