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MiRNA profile of lung adenocarcinoma cells treatment with monoclonal antibody NJ001 [miRNA_72h]

ABSTRACT: Previously, we developed a newly monoclonal antibody named NJ001 which selectively reacted to non-small cell lung cancer and exhibited anti-tumor activity both in vitro and in vivo by inhibiting proliferation, colony formation, apoptosis and so on. MiRNA ubiquitously regulates cell processes such as cell cycle regulation, invasion, differentiation and proliferation. We used microarrays to detail the miRNA changes in the lung adenocarcinoma cell SPC-A1 after treatment with NJ001. These miRNA may have contribution to the effect of NJ001 on cancer cells.

ORGANISM(S): synthetic construct Homo sapiens

PROVIDER: GSE51945 | GEO | 2016/10/29

SECONDARY ACCESSION(S): PRJNA225912

REPOSITORIES: GEO

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miRNA profile of lung adenocarcinoma cells treatment with monoclonal antibody NJ001 [miRNA_12h_24h_48h]

Project description:Previously, we developed a newly monoclonal antibody named NJ001 which selectively reacted to non-small cell lung cancer and exhibited anti-tumor activity both in vitro and in vivo by inhibiting proliferation, colony formation, apoptosis and so on. MiRNA ubiquitously regulates cell processes such as cell cycle regulation, invasion, differentiation and proliferation. We used microarrays to detail the miRNA changes in the lung adenocarcinoma cell SPC-A1 after treatment with NJ001. These miRNA may have contribution to the effect of NJ001 on cancer cells.

2016-10-29 | GSE51946 | GEO

Human Lung Adenocarcinoma Cells: control vs. mAb NJ001 treated

Project description:Transcriptional profiling of human lung adenocarcinoma cells comparing control untreated SPC-A1 cells with SPC-A1 cells treated with 300 M-BM-5g/ml mAb NJ001 for 36h Two-condition experiment, SPC-A1 vs. NJ001-SPC-A1 cells. Biological replicates: 3 control, 3 treated, independently grown and harvested. One replicate per array.

2014-08-01 | E-GEOD-59655 | biostudies-arrayexpress

Human Lung Adenocarcinoma Cells: control vs. mAb NJ001 treated

Project description:Transcriptional profiling of human lung adenocarcinoma cells comparing control untreated SPC-A1 cells with SPC-A1 cells treated with 300 µg/ml mAb NJ001 for 36h

2014-08-01 | GSE59655 | GEO

Hypoxia induced gene expression in lung adenocarcinoma cells

Project description:Two lung adenocarcinoma cell lines, A549 and SPC-A1, were cultured under two different oxygen concentrations, 1% and 20%, respectively. After 24 hours cultured, cells were collected and total RNA was extracted. Affymetrix GeneChip® Gene 1.0 ST Array System for Human was applied to detect the differences of gene expression of lung adenocarcinoma cell lines cultured under different oxygen concentrations (total RNA of the two cells was pooled with equal quantity). The experiments were repeated with the same procedures except culturing tumor cell lines in matrigel.

2015-04-30 | E-MTAB-3512 | biostudies-arrayexpress

Comparative expression of bone metastasis clones and its parental cells on Chinese lung adenocarcinoma cell line SPC-A-1 and human larger cell lung cancer cell line NCI-H460 by cDNA array.

Project description:Chinese lung adenocarcinoma cancer cells (SPC-A-1) and human larger cell lung cancer cells (NCI-H460) were injected into left cardiac ventricle of nude mice for bone metastases model, respectively. Bone metastatic lesions were detected by bone scintigraphy with 99mTc-methylene diphophonate, removed bone metastatic lesions for cell primary culture, chromosome analysis for determine the bone metastatic cells have a characterization of unchanged humanization, in the anesthesia death mice. Through eight in vivo ~ in vitro selections, the 4th, 8th generation cells of SPC-A-1, 8th generation cells of NCI-H460 and their parental cells were used for microarray analysis, respectively. Bone metastatic clones 4th and/or 8th generation SPC-A-1 vs. SPC-A-1, 8th generation NCI-H460 vs. NCI-H460, respectively. Biological replicates: one replicate for every group, independently grown and harvested. One replicate per array.

2017-05-01 | E-GEOD-57402 | biostudies-arrayexpress

Monoclonal Antibody Targeting Pear1 for Pulmonary Fibrosis Therapy [scRNA-seq]

Project description:Pulmonary fibrosis (PF) is a chronic interstitial lung disease that causes irreversible and progressive lung scarring and respiratory failure. Activation of fibroblasts (FBs) play a central role in progression of PF. Here we report that platelet endothelial aggregation receptor 1 (Pear1) in FBs is a new molecular target for PF therapy. Pear1 deficiency spontaneously caused respiratory function decline and alveolar collagens accumulation in old mice. The degree of PF and mortality induced by bleomycin were significantly enhanced in Pear1 deficient mice. FB Mesenchyme-specific Pear1 deficiency aggravated bleomycin-induced PF, confirming that Pear1 modulates PF progression probably byvia regulation of FBs function. Single cell RNA-seq analysis of pulmonary FB and functional enrichment analysis revealed drastic expansion of Aactivated- FB clusters and enrichment of activated FB marker genes in extracellular matrix (ECM) development and pulmonary fibrosis in Pear1-/- fibrotic lungs. CD140+ bulk tissue RNA-seq analysis further confirmed that multiple mesenchyme development pathways especially epithelial mesenchymal transition (EMT) are enriched with up-regulated genes involving FB mediated ECM organization and development in in Pear1-/- fibrotic lungs. We further found that Pear1 associated with Protein Phosphatase 1 to suppress fibrotic factors such as TGFß, FGF or PDGF-induced intracellular signalling and FB activation. Intratracheal aerosolization of monoclonal antibody activating Pear1 greatly ameliorates PF in both wild-type mice and Pear1-humanized mice, suggesting that targeting Pear1 may serve as a new therapeutic strategy for PF.

2021-10-20 | GSE183545 | GEO

Lung inflammatory milieu in mice with chronic CD4+ T cell mediated auto-immune inflammation of the lung

Project description:Noncommunicable chronic respiratory diseases (CRDs) such as chronic obstructive pulmonary disease (COPD) and asthma affect hundreds of millions of people and are associated with increasing morbidity and mortality. CRDs are multifactorial disorders and despite different etiologies they commonly manifest in pulmonary structural (airway remodeling, emphysema) and/or functional changes. In this study we used mice intrinsically developing autoimmune-mediated lung inflammation associated with lung pathology and immune imprinting partly comparable to hallmarks of CRD. The so called SPC-HAxTCR-HA transgenic mice (BALB/c genetic background), express a neo-self antigen (influenza A virus hemagglutinin, HA) on lung alveolar epithelial type II cells in the presence of HA-specific CD4+ T cells leading to the establishment of chronic lung inflammation. In order to characterize the inflammatory lung milieu of SPC-HAxTCR-HA mice in comparison to SPC-HA control mice (lacking HA-specific CD4+ T cells), we performed whole lung tissue transcriptional analyses (n = 3 / group). 378 transcripts were found to be differentially expressed in SPC-HAxTCR-HA lungs. 326 of those were up-regulated and 52 were down-regulated compared to SPC-HA control mice.

2016-12-31 | GSE66531 | GEO

Scavenger Receptor A1 Prevents Non-Small Cell Lung Cancer Metastasis by Suppressing Macrophage Serum Amyloid A1 Expression

Project description:Metastasis is the key determinant of poor prognosis for advanced-stage NSCLC patients. Although an important contributor to metastasis is cross-talk between tumor-associated macrophages (TAMs) and tumor cells, its regulation is not fully understood. Expressed primarily in macrophages, scavenger receptor A1 (SR-A1) has been associated with lung tumorigenesis. Here, the mechanistic basis for the involvement of SR-A1 in lung cancer prognosis was investigated using population genetics, transcriptomics, and functional analyses. SR-A1 genetic variants were investigated for possible association with survival of advanced-stage NSCLC patients in the Harvard Lung Cancer Study cohort. Two SNPs (rs17484273, rs1484751) in SR-A1 were significantly associated with poor overall survival of NSCLC patients. Further, data from The Cancer Genome Atlas showed a considerable down-regulation of SR-A1 in lung tumor tissues. The association of SR-A1 with prognosis was validated in animal models in the context of lung cancer metastasis. Macrophages derived from SR-A1 knockout mice accelerated metastasis in a lung cancer mouse model. On the other hand, tumor cell seeding, migration, and invasion as well as macrophage accumulation in lung cancer tissue were enhanced in SR-A1 knockout mice. Furthermore, SR-A1 deficiency promoted up-regulation of serum amyloid A1 (SAA1) in macrophages, which appeared to be mediated by MAPK/Ikappa-B/NF-kappaB signaling. Further, SAA1 exposure promoted tumor cell invasion and macrophage migration in vitro and in vivo, but these effects were blocked by administration of an anti-SAA1 antibody. These findings suggest that SR-A1 may suppress lung cancer metastasis by down-regulating SAA1 production in macrophages.

2019-06-16 | GSE83473 | GEO

Monoclonal Antibody Targeting Pear1 for Pulmonary Fibrosis Therapy [bulk RNA-seq]

2021-10-20 | GSE183657 | GEO

Expression data from mouse lung alveolar epithelial type II cell with Yap/Taz deletion after bacterial pneumonia-induced lung injury

Project description:To define the role of Yap/Taz in alveolar epithelial regeneration, we deleted Yap/Taz in mouse lung Spc-expressing ATII cells by using Spc-CreERT2, Yap fl/fl, Taz fl/fl, R26R-mTmG mice. This data set contains the microarrays examining gene expression in the lineage-labeled Spc-expressing ATII cells before and after Streptococcus pneumoniae infection.

2018-12-01 | GSE86027 | GEO

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