Gene expression profiling of mouse osteotropic lung cancer cells
Ontology highlight
ABSTRACT: Analysis of gene expression profiling in osteotropic Lewis Lung carcinoma cells. The osteotropic lung cancer cell sublines were established throuth in vivo selection. The gene expression profiling of parental and osteotropic sublines was identified through microarray analysis.
Project description:Purpose: To study the alteration of whole transcriptome of Lewis lung carcinoma (LLC) cells after the decreasing of malignant properties of tumor by treatment of tumor-bearing mice with RNase A. Methods: Whole transcriptome profile of Lewis lung carcinoma before and after RNase A treatment were generated by deep sequencing using SOLiD 5.5. The sequence reads were mapped by Bioscope 1.3 software, differential expression was evaluated by Cufflinks v.2.0.1 package. Results: Difference in expression was found for 966 genes. Conclusions: Our study represents the first detailed analysis of alteration of transcriptome of Lewis lung carcinoma after the decrease of malignant prtoperties of the tumor (proliferation and invasion) by RNase A. Whole transcriptome profile of Lewis lung carcinoma before and after RNase A treatment were generated by deep sequencing using SOLiD 5.5.
Project description:Purpose: To study the alteration of whole transcriptome of Lewis lung carcinoma (LLC) cells after the decreasing of malignant properties of tumor by treatment of tumor-bearing mice with RNase A. Methods: Whole transcriptome profile of Lewis lung carcinoma before and after RNase A treatment were generated by deep sequencing using SOLiD 5.5. The sequence reads were mapped by Bioscope 1.3 software, differential expression was evaluated by Cufflinks v.2.0.1 package. Results: Difference in expression was found for 966 genes. Conclusions: Our study represents the first detailed analysis of alteration of transcriptome of Lewis lung carcinoma after the decrease of malignant prtoperties of the tumor (proliferation and invasion) by RNase A.
Project description:To investigate the interaction between lung cancer cell and lung fibrosis in vivo, gene expression analysis was performed using orthotopic tumor bearing animal model with C57BL/6 mice and Lewis Lung Carcinoma cells (LC model) and LC model with bleomycin-induced lung fibrosis (IP+LC model).
Project description:Smoking is the most important risk factor for both lung cancer (LC) and chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the role of myeloid cell NF-kB in the regulation of tumor cell growth signaling. We subjected mice lacking myeloid RelA/p65 to a metastatic LC model. Cigarette smoke (CS) exposure significantly increased the proliferation of Lewis lung carcinoma cell (LLC) tumors in wild type mice. In CS exposed mice lacking myeloid RelA/p65, the tumor growth was largely inhibited. Transcriptome and pathway analysis of cancer tissue revealed a fundamental impact of myeloid cells on various growth signaling pathways. Myeloid RelA/p65 is necessary to link smoke-induced inflammation with LC growth. Keywords: Expression profiling by array Analysis of gene expression in lewis lung carcinoma cells resected from lungs of WT and RelA/p65 deficient mice exposed to smoke or air. Four different samples were analyzed (3 replicates each).
Project description:To investigate the interaction between lung alveolar macrophages and lung cancer cells in vivo, gene expression analysis was performed using orthotopic tumor bearing animal model with C57BL/6 mice and Lewis Lung Carcinoma (LLC) cells. CD45+, F4/80+, Siglec-F+ population was sorted as alveolar macrophage population with fluorescence-activated cell sorting (FACS) technique.
Project description:To classify the cell population of lung alveolar macrophages in the presence (or absence) of lung cancer cells in vivo, single cell RNA sequence analysis was performed using orthotopic tumor bearing animal model with C57BL/6 mice and Lewis Lung Carcinoma (LLC) cells. CD45+, F4/80+, Siglec-F+ population was sorted as alveolar macrophage population with fluorescence-activated cell sorting (FACS) technique.
Project description:Radiotherapy is one of the most common therapies for cancer. Approximately half of all cancer patients will receive radiotherapy at some point during treatment. Consequences of IR treatment are dose dependent and different sensitivity to IR of various types of cells is well established. To reduce the damage of IR to most sensitive cells of normal (noncancerous) tissue radiotherapy is administered as fractionated dose treatment applying radiation in ~2 Gy fractions every 24 hours, 5 times per week. However, during the therapy intrinsic and acquired tumor radioresistance may result in treatment failures. Comprehensive mechanisms of the resistance to irradiation as well as mechanisms of cellular response to fractionated dose IR remain unclear. Therefore, in the present study we evaluated global gene expression changes in murine Lewis lung carcinoma LLC1 cells following X-ray irradiation of single 2 Gy or 10 Gy and 2 Gy x 5 fractionated doses. Total RNA was harvested from mouse Lewis lung carcinoma cells 4h after treatment of single (2 Gy or 10 Gy) or fractionated (5x2 Gy) ionizing radiation dose.
Project description:Three isogenic HNC cell sublines with highly invasive properties were established. Invasion-associated genes were identified by comparison of transcriptomic profiles between HNC parental cell lines and the invasive sublines via Affymetrix cDNA microarrays. We used cDNA microarray to compare gene expression of invasion subline cells and parental cells in head and neck cancer.