Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
The University of Texas, The Graduate School of Biomedical Sciences, Houston, Texas.
Cancer Discov. 2019 Feb;9(2):173-175. doi: 10.1158/2159-8290.CD-18-1460.
In this issue of , Biffi and colleagues report that IL1 signaling cascades resulted in JAK/STAT activation and promoted an inflammatory cancer-associated fibroblast (iCAF) state, which contributed to the establishment of distinct fibroblast niches in the pancreatic ductal adenocarcinoma (PDAC) microenvironment to support the growth of PDAC cells. Furthermore, the investigators demonstrated that TGFβ signaling inhibited IL1R1 expression, antagonized IL1α responses, and promoted differentiation of CAFs into myofibroblasts; thus, IL1α signaling is an important therapeutic target for both PDAC cells and the iCAFs in the tumor microenvironment..
本期的 杂志中，Biffi 及其同事报告称，IL1 信号级联导致了 JAK/STAT 的激活，并促进了炎症相关的癌性成纤维细胞（iCAF）状态，这有助于在胰腺导管腺癌（PDAC）微环境中建立独特的成纤维细胞小生境，以支持 PDAC 细胞的生长。此外，研究人员还表明，TGFβ信号抑制了 IL1R1 的表达，拮抗了 IL1α 的反应，并促进了 CAFs 向肌成纤维细胞的分化；因此，IL1α 信号是 PDAC 细胞和肿瘤微环境中的 iCAFs 的一个重要治疗靶点。
