scholarly journals Spi-B Promotes the Recruitment of Tumor-Associated Macrophages via Enhancing CCL4 Expression in Lung Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Qiumin Huang ◽  
Junrong Liu ◽  
Shuainan Wu ◽  
Xuexi Zhang ◽  
Zengtuan Xiao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Microenvironment ◽  
Human Lung ◽  
Immune Escape ◽  
Critical Role ◽  
Human Lung Cancer ◽  
Clinical Samples ◽  
Tumor Associated Macrophages ◽  
Tumor Immune Escape ◽  
Anticancer Immunotherapy

Tumor immune escape plays a critical role in malignant tumor progression and leads to the failure of anticancer immunotherapy. Spi-B, a lymphocyte lineage-specific Ets transcription factor, participates in mesenchymal invasion and favors metastasis in human lung cancer. However, the mechanism through which Spi-B regulates the tumor immune environment has not been elucidated. In this study, we demonstrated that Spi-B enhanced the infiltration of tumor-associated macrophages (TAMs) in the tumor microenvironment using subcutaneous mouse models and clinical samples of human lung cancer. Spi-B overexpression increased the expression of TAM polarization- and recruitment-related genes, including CCL4. Moreover, deleting CCL4 inhibited the ability of Spi-B promoting macrophage infiltration. These data suggest that Spi-B promotes the recruitment of TAMs to the tumor microenvironment via upregulating CCL4 expression, which contributes to the progression of lung cancer.

scholarly journals Atypical Protein Kinase Cι Plays a Critical Role in Human Lung Cancer Cell Growth and Tumorigenicity

2005 ◽  
Vol 280 (35) ◽  
pp. 31109-31115 ◽  
Author(s):  
Roderick P. Regala ◽  
Capella Weems ◽  
Lee Jamieson ◽  
John A. Copland ◽  
E. Aubrey Thompson ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Lung ◽  
Critical Role ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cell

scholarly journals Molecular Determinants of AHPN (CD437)-Induced Growth Arrest and Apoptosis in Human Lung Cancer Cell Lines

1998 ◽  
Vol 18 (8) ◽  
pp. 4719-4731 ◽  
Author(s):  
Yin Li ◽  
Bingzhen Lin ◽  
Anissa Agadir ◽  
Ru Liu ◽  
Marcia I. Dawson ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Lung ◽  
Critical Role ◽  
Cancer Cell Lines ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Human Lung Cancer Cell ◽  
Induced Apoptosis

ABSTRACT 6-[3-(1-Adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (AHPN or CD437), originally identified as a retinoic acid receptor γ-selective retinoid, was previously shown to induce growth inhibition and apoptosis in human breast cancer cells. In this study, we investigated the role of AHPN/CD437 and its mechanism of action in human lung cancer cell lines. Our results demonstrated that AHPN/CD437 effectively inhibited lung cancer cell growth by inducing G0/G1 arrest and apoptosis, a process that is accompanied by rapid induction of c-Jun, nur77, and p21 WAF1/CIP1 . In addition, we found that expression of p53 and Bcl-2 was differentially regulated by AHPN/CD437 in different lung cancer cell lines and may play a role in regulating AHPN/CD437-induced apoptotic process. On constitutive expression of the c-JunAla(63,73) protein, a dominant-negative inhibitor of c-Jun, in A549 cells, nur77 expression and apoptosis induction by AHPN/CD437 were impaired, whereas p21 WAF1/CIP1 induction and G0/G1 arrest were not affected. Furthermore, overexpression of antisense nur77 RNA in A549 and H460 lung cancer cell lines largely inhibited AHPN/CD437-induced apoptosis. Thus, expression of c-Jun and nur77 plays a critical role in AHPN/CD437-induced apoptosis. Together, our results reveal a novel pathway for retinoid-induced apoptosis and suggest that AHPN/CD437 or analogs may have a better therapeutic efficacy against lung cancer.

Abstract 3803: Immune escape from NK cells and activated CD8 T cells by miR-183 repression of MICA/B expression in human lung cancer

2018 ◽  
Author(s):  
Nhan Tu ◽  
Thu Le Trinh ◽  
Sarah S. Donatelli ◽  
Melba M. Tejera ◽  
Danielle L. Gilvary ◽  
...  
Keyword(s):  
Lung Cancer ◽  
T Cells ◽  
Nk Cells ◽  
Cd8 T Cells ◽  
Human Lung ◽  
Immune Escape ◽  
Human Lung Cancer

scholarly journals Human lung cancer antigen presentation by tumor-associated macrophages to CD4+ lymphocytes from regional nodes

1998 ◽  
Vol 7 (1) ◽  
pp. 19-24
Author(s):  
Takashi Yoshimatsu ◽  
Ichiro Yoshino ◽  
Mitsuhiro Takenoyama ◽  
Takeshi Hanagiri ◽  
Hiroshi Fujie ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Antigen Presentation ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Tumor Associated Macrophages ◽  
Cancer Antigen ◽  
Cd4 Lymphocytes

scholarly journals Exosomes Derived from RM-1 Cells Promote the Recruitment of MDSCs into Tumor Microenvironment by Upregulating CXCR4 via TLR2/NF- κ B Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Nan Li ◽  
Yingying Wang ◽  
Haoyu Xu ◽  
Hexi Wang ◽  
Yingying Gao ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Flow Cytometry ◽  
Tumor Microenvironment ◽  
Immune Escape ◽  
Critical Role ◽  
Specific Inhibitor ◽  
Signalling Pathway ◽  
Dependent Manner ◽  
Migration Ability ◽  
Tumor Immune Escape

Myeloid-derived suppressor cells (MDSCs) play a critical role in tumor immune escape because of its remarkable immunosuppressive effect. However, the mechanism of MDSCs migrated into tumor microenvironment remains unclear. In this study, we demonstrated the recruitment of MDSCs can be promoted by exosomes derived from prostate cancer cells, which could upregulate chemokine (CXC motif) receptor 4 (CXCR4) via the TLR2/NF- κ B signalling pathway. Flow cytometry detected that the percentage of MDSCs in the mice spleen and tumor tissue was significantly increased after injection with exosomes via mouse tail vein. Transwell chemotaxis assay showed the recruitment of MDSCs toward the lower chamber was enhanced after stimulation with exosomes, and the migration ability could be inhibited by AMD3100 (a CXCR4 specific inhibitor) both in vivo and in vitro. Additionally, Western blot and flow cytometry verified a remarkably increase of CXCR4 in MDSCs after incubation with exosomes; meanwhile, the protein level of TLR2 and activation of NF- κ B were also strengthened obviously. Nevertheless, after blocking TLR2 by C29 (a TLR2-specific inhibitor), the expression of p-p65 and CXCR4, which were hypothesized as the downstream target of TLR2, was prominently reduced. In conclusion, prostate cancer-derived exosomes could reinforce CXCR4 expression in MDSCs through the TLR2/NF- κ B signalling pathway, eventually promoting migration of MDSCs into tumor microenvironment in a CXCR4-CXCL12 axis-dependent manner.

HO-1 and miR-378 regulate tumor microenvironment and angiogenic potential of human lung cancer

2012 ◽  
Vol 56 (5-6) ◽  
pp. 369
Author(s):  
Klaudia Skrzypek ◽  
Magdalena Tertil ◽  
Slawomir Golda ◽  
Kazimierz Weglarczyk ◽  
Halina Was ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Microenvironment ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Angiogenic Potential

Ras Denitrosylation in Human Lung Cancer

2012 ◽  
Vol 3 (2) ◽  
pp. 135-139
Author(s):  
Benjamin Gaston ◽  
Nadzeya Marozkina
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Human Lung Cancer
Sign in / Sign up

Export Citation Format

Share Document