Similar Datasets
Project description:RNAseq of SCLC cell line H1155 with PAX5.knocked out. The goals of this study are to identify the function of PAX5 in SCLC.
2021-01-31 | GSE135439 | GEO
Project description:Poor prognosis of small cell lung cancer (SCLC) is mainly attributed to its highly metastatic capability. Here we identify the SMC and Non-SMC from Rb1L/L/Trp53 L/L mouse model through FACS with NE and mensenchymal markers. In order to identify functions of these two subpopulations during SCLC malignant progression, we compared their metastatic capability by allograft experiment. In addition, we find that the SMC is progressively transited from the Non-SCLC during mouse SCLC malignant progression. Further investigation reveals that genetic disruption of the SWI/SNF chromatin-remodeling complex, in RP model abrogates SMC phenotype maintenance and SCLC metastasis. In search of important downstream regulators, we find that TAZ, the core transcription cofactor of the Hippo pathway, is epigenetically silenced by SWI/SNF complex during this process. Collectively, our data link phenotypic transition to cancer metastasis and identify TAZ as a critical molecular switch that controls SCLC plasticity.
2022-08-24 | GSE158293 | GEO
Project description:Small cell lung cancer (SCLC) is characterized by significant heterogeneity and plasticity, which contribute to its aggressive progression and resistance to therapy. Understanding the underlying mechanisms of these features is essential for improving treatment outcomes. Autophagy, a conserved cellular process, plays a role in many cancers; however, its specific function in SCLC remains unclear. Utilizing a genetically engineered mouse model (Rb1fl/fl; Trp53fl/fl; GFP-LC3-RFP-LC3△G), we tracked autophagic flux in vivo to assess its effects on SCLC biology. Tumor subpopulations with high autophagic flux exhibited increased proliferation, enhanced metastatic potential, and neuroendocrine (NE) characteristics, whereas those with low autophagic flux displayed more immune-related signals and non-NE traits. In vitro modulation of autophagic flux further corroborated these findings: the autophagy activator trehalose induced NE features in non-NE cell lines (H841), while the autophagy inhibitor Bafilomycin A1 promoted non-NE characteristics in NE cell lines (H1092). This study provides a model for investigating autophagy in vivo and underscores its role in the heterogeneity and plasticity of SCLC.
2024-12-17 | GSE284267 | GEO
Project description:Poor prognosis of small cell lung cancer (SCLC) is mainly attributed to its highly metastatic capability. Here we identify the SMC and Non-SMC from Rb1L/L/Trp53 L/L mouse model through FACS with NE and mensenchymal markers. In order to identify functions of these two subpopulations during SCLC malignant progression, we compared their metastatic capability by allograft experiment. In addition, we find that the SMC is progressively transited from the Non-SCLC during mouse SCLC malignant progression. Further investigation reveals that genetic disruption of the SWI/SNF chromatin-remodeling complex, in RP model abrogates SMC phenotype maintenance and SCLC metastasis. In search of important downstream regulators, we find that TAZ, the core transcription cofactor of the Hippo pathway, is epigenetically silenced by SWI/SNF complex during this process. Collectively, our data link phenotypic transition to cancer metastasis and identify TAZ as a critical molecular switch that controls SCLC plasticity.
2022-08-24 | GSE158091 | GEO
Project description:Analysis of prostate adnocarcinoma cell line LNCaP cells overexpression pair box 5 (PAX5) for up to 4 days. The goals of this study are to compare PAX5 overexpression in LNCaP cell drives transcriptome profiling (RNA-seq) changes.
2021-01-31 | GSE129887 | GEO
Project description:Poor prognosis of small cell lung cancer (SCLC) is mainly attributed to its highly metastatic capability. Here we identify the SMC and Non-SMC from Rb1L/L/Trp53 L/L mouse model through FACS with NE and mensenchymal markers. In order to identify functions of these two subpopulations during SCLC malignant progression, we compared their metastatic capability by allograft experiment. In addition, we find that the SMC is progressively transited from the Non-SCLC during mouse SCLC malignant progression. Further investigation reveals that genetic disruption of the SWI/SNF chromatin-remodeling complex, in RP model abrogates SMC phenotype maintenance and SCLC metastasis. In search of important downstream regulators, we find that TAZ, the core transcription cofactor of the Hippo pathway, is epigenetically silenced by SWI/SNF complex during this process. Collectively, our data link phenotypic transition to cancer metastasis and identify TAZ as a critical molecular switch that controls SCLC plasticity.
2022-08-24 | GSE158290 | GEO
Project description:PAX5 promotes progression of SCLC
| PRJNA558897 | ENA
Project description:Transcriptional profiling of human breast cancer cell line LM2, a subline of MDA-MB-231 highly metastatic to lung when injected to nude mice, to identify the genes that are regulated after the metastasis gene metadherin is knocked down. Keywords: Genetic modification
2008-02-01 | GSE9187 | GEO
Project description:L1 elements are repeat elements known to get activated during hepatocarcinogenesis. We have knocked-down expression of L1 elements using shRNA targeting L1-ORF1 in Huh7 cell line and a control non-targeting cell line was also generated. Influence of L1 knockdown on overall cellular transcritome was then analysed by RNAseq followed by pathway analysis. Overall, a crosstalk between L1 elements and TGFbeta signaling pathway is observed.
2023-01-21 | GSE126615 | GEO
Project description:HCC cancer cells were knocked down of ZFP36L1 using siRNA and RNASeq was done.
2022-01-01 | GSE160343 | GEO