scholarly journals In vitro secretion of cytokines and prostaglandin-E2by monocytes from lung cancer patients

2001 ◽  
Vol 95 (4) ◽  
pp. 243-245 ◽  
Author(s):  
Y.G. TREJO ◽  
R.H. BORDENAVE ◽  
M. BEVIACQUA ◽  
L.S. RUMI
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Lung Cancer Patients

scholarly journals High Level of Staufen1 Expression Confers Longer Recurrence Free Survival to Non-Small Cell Lung Cancer Patients by Promoting THBS1 mRNA Degradation

2021 ◽  
Vol 23 (1) ◽  
pp. 215
Author(s):  
Florence Bonnet-Magnaval ◽  
Leïla Halidou Diallo ◽  
Valérie Brunchault ◽  
Nathalie Laugero ◽  
Florent Morfoisse ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Adhesion ◽  
Cancer Patients ◽  
Cancer Progression ◽  
Rna Binding ◽  
Recurrence Free Survival ◽  
Free Survival ◽  
Lung Cancer Patients

Stau1 is a pluripotent RNA-binding protein that is responsible for the post-transcriptional regulation of a multitude of transcripts. Here, we observed that lung cancer patients with a high Stau1 expression have a longer recurrence free survival. Strikingly, Stau1 did not impair cell proliferation in vitro, but rather cell migration and cell adhesion. In vivo, Stau1 depletion favored tumor progression and metastases development. In addition, Stau1 depletion strongly impaired vessel maturation. Among a panel of candidate genes, we specifically identified the mRNA encoding the cell adhesion molecule Thrombospondin 1 (THBS1) as a new target for Staufen-mediated mRNA decay. Altogether, our results suggest that regulation of THBS1 expression by Stau1 may be a key process involved in lung cancer progression.

Triggering receptor expressed on myeloid cells-2 (TREM-2) elicited by lung cancer cells to facilitate tumor immune evasion.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e22054-e22054 ◽  
Author(s):  
Yinan Yao ◽  
Hequan Li ◽  
Yuehong Wang ◽  
Jianying Zhou
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Immune Escape ◽  
Myeloid Cells ◽  
Mice Model ◽  
Tumor Immune Escape ◽  
Normal Medium ◽  
Lung Cancer Patients ◽  
Tumor Bearing

e22054 Background: More recent evidences have argued that negative regulatory mechanism that serve to impede ongoing immune responses, which gain in interest as a complementary strategy for cancer therapy. Triggering receptor expressed on myeloid cells-2 (TREM-2) restrains phagocytosis of both dendritic cells (DCs) and macrophages(MΦs), and reduces release of inflammatory cytokines through DAP12-mediated inhibitory signal, prompting us to investigate the role of TREM-2 involved in immune dysfunction among tumor-bearing host. Methods: In lung cancer patients, monocytes of peripheral blood were analyzed by flow cytometry and MΦs around tumour cells in lung tissue were detected by immunehistochemistry. Then we prepared conditional medium containing supernatant of 3LL cells mimicing tumor microenvironment for DC and MΦ derivation, and established an orthotopic lung cancer-bearing mice model to explore the further mechanism. Results: It was showed that TREM-2 expression on monocytes was up-regulated in lung cancer patients compared with that of healthy controls, and that TREM-2 levels of macrophages had a positive correlation with TNM stage. Moreover, reduction of tumor burden, by operation or chemotherapy, led to obvious decline of TREM-2 expression. The percentage of TREM-2+DC in the murine lung significantly increased after tumor-bearing, and such DCs preformed lower MHCII-Ia, CD86 expression, and IL-12 production, but higher IL-10 secretion. In vitro, more TREM-2+DCs and TREM-2+MΦs were harvested from ‘conditional’ medium instead of ‘normal’ medium. Also, TREM-2+DCs rather than TREM-2- DCs markedly inhibited proliferation of T cells, which could be partially abolished by anti-TREM-2 mAb. Conclusions: TREM-2 acts as a negative immune regulator in promoting lung cancer progress. Our study provides new mechanism for tumor immune escape and inhibitory checkpoint for immunotherapy.

scholarly journals MicroRNA-421 confers paclitaxel resistance by binding to the KEAP1 3′UTR and predicts poor survival in non-small cell lung cancer

2019 ◽  
Vol 10 (11) ◽  
Author(s):  
Fu-Gang Duan ◽  
Mei-Fang Wang ◽  
Ya-Bing Cao ◽  
Dan Li ◽  
Run-Ze Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Patients ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Lung Cancer Patients

Abstract MicroRNAs regulate post-transcriptional gene expression and play important roles in multiple cellular processes. In this study, we found that miR-421 suppresses kelch-like ECH-associated protein 1(KEAP1) expression by targeting its 3′-untranslated region (3′UTR). A Q-PCR assay demonstrated that miR-421 is overexpressed in non-small cell lung cancer (NSCLC), especially in A549 cells. Consistently, the level of miR-421 was higher in clinical blood samples from lung cancer patients than in those from normal healthy donors, suggesting that miR-421 is an important lung cancer biomarker. Interestingly, overexpression of miR-421 reduced the level of KEAP1 expression, which further promoted lung cancer cell migration and invasion, as well as inhibited cell apoptosis both in vivo and in vitro. Furthermore, knockdown of miR-421 expression with an antisense morpholino oligonucleotide (AMO) increased ROS levels and treatment sensitivity to paclitaxel in vitro and in vivo, indicating that high miR-421 expression may at least partly account for paclitaxel tolerance in lung cancer patients. To find the upstream regulator of miR-421, one of the candidates, β-catenin, was knocked out via the CRISPR/Cas9 method in A549 cells. Our data showed that inhibiting β-catenin reduced miR-421 levels in A549 cells. In addition, β-catenin upregulation enhanced miR-421 expression, indicating that β-catenin regulates the expression of miR-421 in lung cancer. Taken together, our findings reveal the critical role of miR-421 in paclitaxel drug resistance and its upstream and downstream regulatory mechanisms. Therefore, miR-421 may serve as a potential molecular therapeutic target in lung cancer, and AMOs may be a potential treatment strategy.

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