Liu Sandy T, Pham Hung, Pandol Stephen J, Ptasznik Andrzej
Department of Medicine, Cedars-Sinai Medical Center Los Angeles, CA, USA ; Department of Medicine, David Geffen School of Medicine, University of California-Los Angeles CA, USA.
Department of Medicine, Cedars-Sinai Medical Center Los Angeles, CA, USA.
Front Physiol. 2014 Jan 16;4:416. doi: 10.3389/fphys.2013.00416. eCollection 2013.
Although a causal link between chronic inflammation and cancer has been established, the exact molecular mechanism linking inflammation to cancer remains largely unknown. It was previously postulated that molecular switches responsible for cancer cell development, and for infiltration of inflammatory cells into cancer, were divided into a distinct set of intracellular proteins and signaling pathways. However, recent evidence suggests that both tumor cells and tumor-infiltrating immune cells utilize the same kinases, mostly that of Src family, to facilitate cancer development and progression. In the past few years several groups have found that Src activation both in cancer and inflammatory cells is mainly driven by pro-inflammatory cytokines within the tumor microenvironment. Here we evaluate the cross talks between Src kinase pathways in immune cells and cancer cells. We conclude that Src might serve as a critical mechanistic link between inflammation and cancer, mediating and propagating a cycle between immune and tissue cells that can ultimately lead to the development and progression of cancer.
尽管慢性炎症与癌症之间的因果联系已经确立，但将炎症与癌症联系起来的确切分子机制在很大程度上仍然未知。以前曾推测，负责癌细胞发育以及炎症细胞浸润到癌症中的分子开关被分为一组独特的细胞内蛋白质和信号通路。然而，最近的证据表明，肿瘤细胞和肿瘤浸润免疫细胞都利用相同的激酶，主要是Src家族的激酶，来促进癌症的发展和进展。在过去几年中，几个研究小组发现，癌症和炎症细胞中的Src激活主要由肿瘤微环境中的促炎细胞因子驱动。在这里，我们评估免疫细胞和癌细胞中Src激酶途径之间的相互作用。我们得出结论，Src可能作为炎症与癌症之间的关键机制联系，介导并传播免疫细胞与组织细胞之间的循环，最终可能导致癌症的发展和进展。
