车站3
生物
癌症研究
细胞凋亡
腺癌
祖细胞
基因沉默
体内
癌变
细胞生长
免疫学
癌症
细胞生物学
干细胞
基因
生物技术
生物化学
遗传学
作者
Qian‐Wen Zheng,Qian‐Zhi Ni,Bing Zhu,Xin Liang,Ning Ma,Yikang Wang,Sheng Xu,Hui‐Jun Cao,Xia Ji,Feng-Kun Zhang,Er‐Bin Zhang,Xiaosong Qiu,Xue Ding,Lin Qiu,Xilin Zhang,Zhaohui Dong,Zhigang Li,Xue-Li Zhang,Dong Xie,Jing-Jing Li
出处
期刊:Oncogene
[Springer Nature]
日期:2022-07-29
卷期号:41 (36): 4244-4256
被引量:7
标识
DOI:10.1038/s41388-022-02418-3
摘要
Lung cancer is the most common malignancy and the leading cause of cancer death worldwide, and lung adenocarcinoma (LUAD) is the most prevalent subtype. Considering the emergence of resistance to therapies, it is urgent to develop more effective therapies to improve the prognosis. Here we reported that pancreatic progenitor cell differentiation and proliferation factor (PPDPF) deficiency inhibited LUAD development both in vitro and in vivo. Mechanistically, PPDPF induces hyperactive STAT3 by interfering STAT3-PTPN1 interaction. Activated STAT3 promoted BMPR2 transcription, which further inhibited apoptosis. Moreover, PPDPF reduced NK cell infiltration and activation to develop an immunosuppressive microenvironment, which was also mediated by STAT3. Furthermore, we identified that the expression of PPDPF was positively correlated with the malignant features of LUAD, as well as BMPR2 and p-STAT3 level in clinical samples. Therefore, our study suggests that PPDPF positively regulates BMPR2 expression and facilitates immune escape via regulating STAT3 activity, providing a potential therapy target for LUAD.
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