Circ-METTL15 contributes to the proliferation, metastasis, immune escape and restrains apoptosis in lung cancer by regulating miR-1299/PDL1 axis

Autoimmunity ◽  
2021 ◽  
pp. 1-13
Author(s):  
Rui Zhang ◽  
Liang Shang ◽  
Jinniang Nan ◽  
Kai Niu ◽  
Jixin Dai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Immune Escape

scholarly journals Exosomal PD-L1 promotes tumor growth through immune escape in non-small cell lung cancer

2019 ◽  
Vol 51 (8) ◽  
pp. 1-13 ◽  
Author(s):  
Dong Ha Kim ◽  
HyeongRyul Kim ◽  
Yun Jung Choi ◽  
Seon Ye Kim ◽  
Jung-Eun Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Immune Escape ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals EGFR-TKI resistance promotes immune escape in lung cancer via increased PD-L1 expression

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Shunli Peng ◽  
Rong Wang ◽  
Xiaojuan Zhang ◽  
Yueyun Ma ◽  
Longhui Zhong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Immune Escape ◽  
Objective Response ◽  
Tki Resistance ◽  
Before And After ◽  
Cytotoxicity Of Lymphocytes ◽  
Egfr Tki ◽  
Egfr T790m ◽  
Egfr Tkis

Abstract Background The ATLANTIC trial reported that higher PD-L1 expression in tumors was involved in a higher objective response in patients with EGFR+/ALK+ non-small cell lung cancer (NSCLC), indicating the possibility of anti-PD-1/PD-L1 therapy as a third-line (or later) treatment for advanced NSCLC. Therefore, the determination of status and regulatory mechanisms of PD-L1 in EGFR mutant NSCLC before and after acquired EGFR-TKIs resistance are meaningful. Methods The correlation among PD-L1, c-MET, and HGF was analyzed based on TCGA datasheets and paired NSCLC specimens before and after acquired EGFR-TKI resistance. EGFR-TKI resistant NSCLC cells with three well-known mechanisms, c-MET amplification, hepatocyte growth factor (HGF), and EGFR-T790M, were investigated to determinate PD-L1 expression status and immune escape ability. PD-L1-deleted EGFR-TKIs sensitive and resistant cells were used to evaluate the immune escape ability of tumors in mice xenograft models. Results Positive correlations were found among PD-L1, c-MET, and HGF, based on TCGA datasheets and paired NSCLC specimens. Moreover, the above three resistant mechanisms increased PD-L1 expression and attenuated activation and cytotoxicity of lymphocytes in vitro and in vivo, and downregulation of PD-L1 partially restored the cytotoxicity of lymphocytes. Both MAPK and PI3K pathways were involved in the three types of resistance mechanism-induced PD-L1 overexpression, whereas the NF-kappa B pathway was only involved in T790M-induced PD-L1 expression. Conclusions HGF, MET-amplification, and EGFR-T790M upregulate PD-L1 expression in NSCLC and promote the immune escape of tumor cells through different mechanisms.

Foxp3 in Lewis Lung Cancer Cells Enhances the Expression of TGF-β1 and IL-10

2014 ◽  
Vol 998-999 ◽  
pp. 252-255
Author(s):  
Li Song Chen ◽  
Xiao Dong Gai ◽  
Chun Li
Keyword(s):  
Lung Cancer ◽  
Immune Escape ◽  
Lewis Lung ◽  
Rt Pcr ◽  
Vector Group ◽  
Lewis Lung Cancer ◽  
Tumor Immune Escape ◽  
Empty Vector ◽  
Tgf Β1 ◽  
Empty Vector Group

In order to explore the related mechanism of Foxp3 in tumor immune escape, the study detected the expression of Foxp3 in lewis lung cancer (LLC) cells and analyzed the expression of TGF-β1 and IL-10 in Foxp3 overexpressed LLC cells. Foxp3 mRNA was detected in LLC cells by RT-PCR. Foxp3 was highly expressed in Foxp3 transfected LLC group than that of in empty vector group and LLC group by RT-PCR(P <0.01). The mRNA and protein expression of TGF-β1 and IL-10 significantly increased in Foxp3 transfected LLC group than that of in empty vector group and LLC group by RT-PCR and ELISA(P <0.05). These results suggest that Foxp3 in LLC cells may promote tumor immune escape by enhancing the expression of TGF-β1 and IL-10.

The immune checkpoint, HVEM may contribute to immune escape in non-small cell lung cancer lacking PD-L1 expression

Lung Cancer ◽  
2018 ◽  
Vol 125 ◽  
pp. 115-120 ◽  
Author(s):  
Shengxiang Ren ◽  
Qinrui Tian ◽  
Nadav Amar ◽  
Hui Yu ◽  
Christopher J. Rivard ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Immune Checkpoint ◽  
Immune Escape ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals LINC01140 promotes the progression and tumor immune escape in lung cancer by sponging multiple microRNAs

2021 ◽  
Vol 9 (8) ◽  
pp. e002746
Author(s):  
Rongmu Xia ◽  
Guojun Geng ◽  
Xiuyi Yu ◽  
Zhong Xu ◽  
Jing Guo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Immune Escape ◽  
Direct Interaction ◽  
Cell Counting ◽  
Tumor Xenograft ◽  
Migration And Invasion ◽  
Tumor Immune Escape ◽  
Expression Levels ◽  
Immunodeficient Mice

BackgroundLong intergenic non-protein coding RNA 1140 (LINC01140), a long non-coding RNA, is highly expressed in various cancers; however, its biological functions in lung cancer (LC) progression and immune escape are still unclear.MethodsHere, to elucidate LINC01140 function, 79 paired LC and paracancerous tissues were collected. LINC01140 expression levels were determined using fluorescence in situ hybridization and qPCR analysis. Cell counting kit-8 (CCK-8) assay and transwell assays were performed. The interaction between microRNAs (miRNAs) and LINC01140 was confirmed using an RNA immunoprecipitation assay. Cytokine-induced killer (CIK) cell phenotypes were analyzed by flow cytometry. Cytokine secretion levels were determined by ELISA. CIK cytotoxicity was assessed by measuring lactate dehydrogenase release. Besides, xenograft tumor mouse models were used to unveil the in vivo function of LINC01140.ResultsWe found that LINC01140 was highly expressed in human LC tissues and cell lines. High LINC01140 levels were associated with poor survival in patients with LC. LINC01140 upregulation promoted the proliferation, migration, and invasion of LC cells through direct interaction with miR-33a-5p and miR-33b-5p, thereby contributing to c-Myc expression and also inhibited cisplatin-induced cell apoptosis. In subcutaneous tumor xenograft mice, LINC01140 knockdown markedly reduced tumor growth and lung metastasis. Additionally, LINC01140 directly repressed miR-377-3 p and miR-155-5 p expression levels, resulting in the upregulation of their common downstream target programmed death-ligand 1 (PD-L1), a crucial target in LC immunotherapy. Notably, we proved that LINC01140 knockdown, along with CIK administration, suppressed the growth of subcutaneous LC xenografts by decreasing PD-L1 expression in severe combined immunodeficient mice.ConclusionsTaken together, LINC01140 overexpression protects c-Myc and PD-L1 mRNA from miRNA-mediated inhibition and contributes to the proliferation, migration, invasion, and immune escape of LC cells. These results provide a theoretical basis that LINC01140 is a promising target for LC treatment.

scholarly journals Nivolumab monotherapy or combination therapy with ipilimumab for lung cancer: a systemic review and meta-analysis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Huihui Jiang ◽  
Aiqun Xu ◽  
Wanli Xia ◽  
Xingyuan Xia ◽  
Pulin Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Monoclonal Antibody ◽  
Combination Therapy ◽  
Immune Escape ◽  
Human Life ◽  
Objective Response ◽  
Progression Free Survival ◽  
Systemic Review ◽  
Advanced Lung Cancer ◽  
Incidence And Mortality

Abstract Background The high incidence and mortality of lung cancer have seriously affected human life and health. Nivolumab is a monoclonal antibody that can inhibit programmed death 1 (PD-1) and Ipilimumab is a monoclonal antibody against CTLA-4(cytotoxic T lymphocyte-associated antigen 4), both of which can prevent the immune escape of tumor cells. Our goal was to synthesize evidence from published randomized controlled trials involving the safety and efficacy of either Nivolumab alone or in combination for the treatment of unresectable lung cancer. Methods We searched the following electronic databases: PubMed, Embase, and Cochrane libraries, and screened the retrieved records for eligibility. We used the Stata16 software for the analyses. The results of the analysis are expressed as hazard ratios (HRs) or risk ratios (RRs) and their corresponding 95% confidence intervals (CI). Results The final analysis included seven trials involving 3817 patients. Among patients with advanced lung cancer, patients using immunotherapy had better overall survival (OS), progression-free survival (PFS), and an objective response rate (ORR) than patients receiving chemotherapy. The HR of Nivolumab monotherapy or combination therapy with OS was compared with that of chemotherapy (HR: 0.73, 95% CI 0.64–0.83; HR: 0.67, 95% CI 0.55–0.81), and the HR of PFS was (HR: 0.81, 95% CI 0.69–0.94; HR: 0.67, 95% CI 0.55–0.82). Conclusions Immunotherapy has been shown to have more clinically meaningful survival benefits for patients with lung cancer, whether monotherapy or combination immunotherapy. CRD42020213440

Sign in / Sign up

Export Citation Format

Share Document