Bruno Antonino, Pagani Arianna, Pulze Laura, Albini Adriana, Dallaglio Katiuscia, Noonan Douglas M, Mortara Lorenzo
Scientific and Technology Pole, IRCCS MultiMedica , Milan , Italy.
Department of Biotechnology and Life Sciences, University of Insubria , Varese , Italy.
Front Oncol. 2014 Jul 2;4:131. doi: 10.3389/fonc.2014.00131. eCollection 2014.
It is widely accepted that the tumor microenvironment (TUMIC) plays a major role in cancer and is indispensable for tumor progression. The TUMIC involves many "players" going well beyond the malignant-transformed cells, including stromal, immune, and endothelial cells (ECs). The non-malignant cells can acquire tumor-promoting functions during carcinogenesis. In particular, these cells can "orchestrate" the "symphony" of the angiogenic switch, permitting the creation of new blood vessels that allows rapid expansion and progression toward malignancy. Considerable attention within the context of tumor angiogenesis should focus not only on the ECs, representing a fundamental unit, but also on immune cells and on the inflammatory tumor infiltrate. Immune cells infiltrating tumors typically show a tumor-induced polarization associated with attenuation of anti-tumor functions and generation of pro-tumor activities, among these angiogenesis. Here, we propose a scenario suggesting that the angiogenic switch is an immune switch arising from the pro-angiogenic polarization of immune cells. This view links immunity, inflammation, and angiogenesis to tumor progression. Here, we review the data in the literature and seek to identify the "conductors" of this "orchestra." We also suggest that interrupting the immune → inflammation → angiogenesis → tumor progression process can delay or prevent tumor insurgence and malignant disease.
肿瘤微环境(TUMIC)在癌症中起主要作用且对肿瘤进展不可或缺,这一点已被广泛接受。肿瘤微环境涉及许多“参与者”,远远超出恶性转化细胞,包括基质细胞、免疫细胞和内皮细胞(ECs)。非恶性细胞在致癌过程中可获得促肿瘤功能。特别是,这些细胞能够“编排”血管生成开关的“交响乐”,促使生成新血管,从而使肿瘤能够快速扩张并向恶性发展。在肿瘤血管生成的背景下,相当多的关注不仅应集中在作为基本单位的内皮细胞上,还应关注免疫细胞和肿瘤炎性浸润。浸润肿瘤的免疫细胞通常表现出肿瘤诱导的极化,这与抗肿瘤功能减弱和促肿瘤活性产生有关,其中包括血管生成。在此,我们提出一种设想,即血管生成开关是由免疫细胞的促血管生成极化引发的免疫开关。这一观点将免疫、炎症和血管生成与肿瘤进展联系起来。在此,我们回顾文献中的数据并试图找出这个“管弦乐队”的“指挥”。我们还认为,中断免疫→炎症→血管生成→肿瘤进展过程可延缓或预防肿瘤发生和恶性疾病。