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: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:This study aimed to elucidate the mechanism by which exosomes from bone-metastatic Lewis lung carcinoma (BM-LLC) cells promote osteolytic metastasis. We performed RNA-seq on mouse RAW264.7 macrophages (osteoclast precursors) treated with exosomes derived from either non-metastatic (NC-LLC) or bone-metastatic (BM-LLC) Lewis lung carcinoma cells. The goal was to identify differentially expressed genes and key regulatory pathways involved in exosome-induced osteoclast differentiation. Integrated analysis with small RNA sequencing data from the exosomes identified the miR-484-PECAM1 axis as a critical driver of this process. Our findings reveal that BM-LLC exosomes deliver miR-484 to recipient macrophages, repress PECAM1 expression, and subsequently upregulate osteoclastogenic markers (TRAP, CTSK, RANKL) and master transcription factors (NFATc1, c-Fos), thereby reprogramming osteoclastogenesis and driving bone destruction.
Project description:We previously identified an extracellular pH-sensing G protein-coupled receptor T cell death associated gene 8 (TDAG8) as an extracellular pH sensor of tumor cells that promotes cell growth/survival in vitro and tumor development in vivo. To determine genes regulated by TDAG8 in vitro, mouse Lewis lung carcinoma (LLC) cells stably expressing TDAG8 (TDAG8-LLC cells) and control vector (control LLC cells) were cultured under acidic conditions. Transcriptome microarray analysis using Affymetrix GeneChip Mouse Genome 430 2.0 Arrays was performed with total RNA prepared from these cells. To determine genes regulated by TDAG8 in vitro, mouse Lewis lung carcinoma (LLC) cells stably expressing TDAG8 (TDAG8-LLC cells) and control vector (control LLC cells) were cultured under acidic conditions. Transcriptome microarray analysis using Affymetrix GeneChip Mouse Genome 430 2.0 Arrays was performed with a mixture of equal amounts of total RNA samples from four independent cell cultures.
Project description:To evaluate the effects of Sildenafil Citrate on the transcriptome, we performed differential gene expression profiling on three different cancer cell lines: 4T1 (breast carcinoma), MC38 (colon adenocarcinoma), and LLC (Lewis lung carcinoma) post-treatment
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.
