MiRNA expression profile of SCLC cell lines vs. normal lung
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE8824 | GEO | 2010/07/24
SECONDARY ACCESSION(S): PRJNA102149
REPOSITORIES: GEO
Similar Datasets
Project description:Aim: To determine the miRNA expression profile of SCLC cell lines vs. normal lung tissue. Keywords: disease state analysis Total RNA isolated from SCLC cell lines H69, HTB-172, HTB-173 and HTB-184 were compared to a mixed RNA sample derived from 6 normal lung tissue samples (fresh surgical material), from 6 tumor-free patients. The same reference sample (normal lung) was used on all 4 microarrays.
2010-07-24 | E-GEOD-8824 | biostudies-arrayexpress
Project description:Aim: To determine the miRNA expression profile of SCLC cell lines vs. normal lung tissue. Keywords: disease state analysis Total RNA isolated from SCLC cell lines H69, HTB-172, HTB-173 and HTB-184 were compared to a mixed RNA sample derived from 6 normal lung tissue samples (fresh surgical material), from 6 tumor-free patients. The same reference sample (normal lung) was used on all 4 microarrays.
| S-ECPF-GEOD-8824 | biostudies-other
Project description:Distinct mRNA populatins have been detected in Epi vs. Mes cells of mouse non-NE SCLC The aim of the study was to globally profile the differential gene expression in Mes vs. Epi cells of mouse non-NE SCLC.
2024-03-11 | GSE168709 | GEO
Project description:Even though small cell lung cancer (SCLC) has entered the age of broad genomic analysis, platinum-based chemotherapy remains the standard care for SCLC. Topotecan is the only approved agent for recurrent or progressive SCLC (1). In the absence of well-defined genomic biomarkers, clinical efficacy signals in genomically distinct subsets of SCLC could have been missed. Serine/Arginine Splicing Factor 1 (SRSF1) is a member of SR protein family. The deleterious consequences of overexpression of the SRSF1 proto-oncogene in human cancers suggest that there are complex mechanisms and pathways underlying SRSF1-mediated transformation (2). Whole exome and transcriptome sequencing of primary tumor SCLC from 99 Chinese patients has identified SRSF1 DNA amplification and mRNA over-expression which predicts poor survival in Chinese SCLC patients. In vitro and in vivo studies have demonstrated that SRSF1 is essential for tumorigenecity of SCLC and plays a key role in DNA repair and chemo-sensitivity. We did RNAseq on 79 small cell lung cancer patients' tumor sample and 7 normal lung tissue. We normalized the RNAseq data and did differential expression analysis. The deleterious consequences of overexpression of the SRSF1 proto-oncogene in human cancers suggest that there are complex mechanisms and pathways underlying SRSF1-mediated transformation.
2016-02-10 | E-GEOD-60052 | biostudies-arrayexpress
Project description:Small cell lungcancer (SCLC) is an aggressive malignancy with dismal clinical outcomes, due inpart to the scarcity of post-relapse tissue samples. To understand more of transcriptional changes associated with treatment resistance, we performed RNAseq analysis of 61 SCLC cell lines.
2020-11-24 | GSE151904 | GEO
Project description:Even though small cell lung cancer (SCLC) has entered the age of broad genomic analysis, platinum-based chemotherapy remains the standard care for SCLC. Topotecan is the only approved agent for recurrent or progressive SCLC (1). In the absence of well-defined genomic biomarkers, clinical efficacy signals in genomically distinct subsets of SCLC could have been missed. Serine/Arginine Splicing Factor 1 (SRSF1) is a member of SR protein family. The deleterious consequences of overexpression of the SRSF1 proto-oncogene in human cancers suggest that there are complex mechanisms and pathways underlying SRSF1-mediated transformation (2). Whole exome and transcriptome sequencing of primary tumor SCLC from 99 Chinese patients has identified SRSF1 DNA amplification and mRNA over-expression which predicts poor survival in Chinese SCLC patients. In vitro and in vivo studies have demonstrated that SRSF1 is essential for tumorigenecity of SCLC and plays a key role in DNA repair and chemo-sensitivity.
2016-02-10 | GSE60052 | GEO
Project description:The human papillomavirus virus (HPV) is a proven cause of most human cervical cancers, and might have a role in other malignancies including vulva, skin, oesophagus, head and neck cancer. HPV has also been speculated to have a role in the pathogenesis of lung cancer. To validate the hypothesis of HPV involvement in small cell lung cancer pathogenesis we performed gene expression profile of transgenic mouse model of SCLC induced by HPV-16 E6/E7 oncoproteins. Gene expression profile of SCLC has been performed using Agilent whole mouse genome (4x44k) representing ~ 41000 genes and mouse transcripts. Samples were obtained from two HPV16-E6/E7 transgenic mouse model and from littermateM-bM-^@M-^Ys normal lung.
2014-05-27 | E-GEOD-23962 | biostudies-arrayexpress
Project description:Small-cell lung cancer (SCLC) is the most fatal form of lung cancer. Intra-tumoral heterogeneity, marked by neuroendocrine (NE) and non-neuroendocrine (non-NE) cell states, defines SCLC, but the drivers of SCLC plasticity are poorly understood. To map the landscape of SCLC tumor microenvironment (TME), we apply spatially resolved transcriptomics and quantitative mass spectrometry-based proteomics to metastatic SCLC tumors obtained via rapid autopsy. The phenotype and overall composition of non-malignant cells in the tumor microenvironment (TME) exhibits substantial variability, closely mirroring the tumor phenotype, suggesting TME-driven reprogramming of NE cell states. We identify cancer-associated fibroblasts (CAF) as a crucial element of SCLC TME heterogeneity, contributing to immune exclusion, and predicting exceptionally poor prognosis. Together, our work provides a comprehensive map of SCLC tumor and TME ecosystems, emphasizing their pivotal role in SCLCs adaptable nature, opening possibilities for re-programming the intercellular communications that shape SCLC tumor states.
2024-05-16 | GSE267560 | GEO
Project description:Drug-tolerant persister cells withstand treatments by adapting their identity through lineage-dependent plasticity during systemic anti-cancer therapies. This phenomenon is evident in small-cell lung carcinoma (SCLC), a lethal neuroendocrine cancer initially responsive (60-80%) to platinum-based chemotherapy but succumbing to resistance within 6 months in advanced stages. This resistance associates with the transdifferentiation of residual tumour cells into a non-neuroendocrine state, a process intricately tied to SCLC's chemotolerance, yet molecular mechanisms governing this lineage conversion remain completed understood. Here we use paired cytoplasmic RNA-seq and polysomal RNA-seq to compare gene expression between NE and non-NE SCLC cell lines on both transcriptional and translational level. We report that first-line chemotherapy induces translation initiation factor eIF6 in drug-tolerant persister-like cells in SCLC, correlating with the non-neuroendocrine state in SCLC. Intervening eIF6 inhibits non-neuroendocrine transdifferentiation, thus enhancing SCLC responsiveness to chemotherapy. This study sheds light on eIF6's potential therapeutic interventions to mitigate treatment resistance in SCLC.
2024-04-30 | GSE262593 | GEO
Project description:Purpose: Small cell lung cancer (SCLC) continues to cause poor clinical outcomes due to limited advances in sustained treatments for rapid cancer cell proliferation and progression. The transcriptional factor Forkhead Box M1 (FOXM1) regulates cell proliferation, tumor initiation and progression in multiple cancer types. However, its biological function and clinical significance in SCLC remain to be established. Hence, the goals of this study are to decipher if FOXM1 is crucial to SCLC cells. Methods: NCI-H1688 stable cells, which contain shFOXM1 or shControl inducible expressing cassette based on pInducer20, plated as triplicates in 60-mm dishes for culturing overnight were induced by doxycycline for 48 hours. Total RNAs were collected by NucleoSpin RNA mini kit and sent for RNA-seq by Novogene. Bioanalyzer 2100 was used to analyze the RNA integrity and cDNA library was constructed with NEBNext UltraTM RNA Library Prep Kit for Illumina. Differential expression gene (DEG) analysis was performed using DESeq2 R package. DEGs were then subjected to ClusterProfiler R package for GO and KEGG enrichment analysis. Results: 1809 downregulated genes and 1781 upregulated genes were enriched in FOXM1-depleted NCI-H1688 cells. SCLC related KEGG pathway was found to be repressed, while multiple cell adhesion and junction associated GOs were induced in FOXM1-depleted NCI-H1688 cells. Furthermore, Foxm1 knockout inhibited SCLC formation in the Rb1fl/flTrp53fl/flMycLSL/LSL (RPM) mouse model associated with increased levels of neuroendocrine markers, Ascl1 and Cgrp, and decrease in Yap1. Consistently, FOXM1 depletion in NCI-H1688 SCLC cells reduced migration and enhanced apoptosis and sensitivity to cisplatin and etoposide. SCLC with high FOXM1 expression (N=30, 57.7%) was significantly correlated with advanced clinical stage, extrathoracic metastases and decrease in overall survival (OS), compared with the low-FOXM1 group (7.90 vs. 12.46 months). Moreover, the high-FOXM1 group showed shorter progression-free survival (PFS), compared with the low-FOXM1 group (3.90 vs. 8.69 months). Our collective findings support the utility of FOXM1 as a prognostic biomarker and potential molecular target for SCLC.
2022-05-01 | GSE174462 | GEO