PD‐L1 / p‐STAT3 promotes the progression of NSCLC cells by regulating TAM polarization

التفاصيل البيبلوغرافية
العنوان: PD‐L1 / p‐STAT3 promotes the progression of NSCLC cells by regulating TAM polarization
المؤلفون: Rui Zhang, Ziqi Meng, Xuwei Wu, Meihua Zhang, Zhengri Piao, Tiefeng Jin
المصدر: Journal of Cellular and Molecular Medicine. 26:5872-5886
بيانات النشر: Wiley, 2022.
سنة النشر: 2022
مصطلحات موضوعية: STAT3 Transcription Factor, Lung Neoplasms, Cell Movement, Carcinoma, Non-Small-Cell Lung, Cell Line, Tumor, Humans, Molecular Medicine, Apoptosis, Cell Biology, B7-H1 Antigen
الوصف: PD-L1 is closely related to the immune escape process of tumour cells, and targeted PD-L1 clinical immunotherapy has been implemented. However, whether PD-L1 is involved in TAM/M2 polarization in the TME of NSCLC and its specific mechanism remain unclear. In order to clarify the specific role of PD-L1 in NSCLC and to seek new treatments for NSCLC, we designed a series of experimental studies. After constructing the co-culture system and conditioned medium system, the proliferation, apoptosis, metastasis, angiogenesis, EMT process and stemness of NSCLC were detected by MTT, flow cytometry, Transwell, endothelial cell tube formation and western blot assays. The results showed that αPD-L1 reversed TAM/M2 polarization by suppressing STAT3 phosphorylation in TAM/M2, therapy inhibiting NSCLC cell migration, angiogenesis, EMT process and stemness. However, αPD-L1 had no effect on the proliferation and apoptosis abilities of NSCLC cells. In vivo experiments showed that αPD-L1 inhibited lung metastasis of NSCLC and reversed TAM/M2 polarization in TME. The study investigates the mechanism by which PD-L1 regulates TAMs polarization in TME and promotes malignant progression of NSCLC, providing a new theoretical basis for PD-L1 targeted therapy of NSCLC.
تدمد: 1582-4934
1582-1838
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d3120f08efc16474c89af301941c4643Test
https://doi.org/10.1111/jcmm.17610Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....d3120f08efc16474c89af301941c4643
قاعدة البيانات: OpenAIRE