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Gene expression profiling data following overexpression of TRIM8 in lung cancer cell lines (A549, CL1-0, H358)

ABSTRACT: Gene expression profiling data following overexpression of TRIM8 in lung cancer cell lines (A549, CL1-0, H358)

PROVIDER: PRJNA953958 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24116249_1.fastq.gz	Fastqsanger.gz
	SRR24116249_2.fastq.gz	Fastqsanger.gz
	SRR24116250_1.fastq.gz	Fastqsanger.gz
	SRR24116250_2.fastq.gz	Fastqsanger.gz
	SRR24116251_1.fastq.gz	Fastqsanger.gz

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Gene expression profiling data following overexpression of TRIM8 in lung cancer cell lines (A549, CL1-0, H358)

Project description:Lung cancer is the cancer with the highest mortality rate in the world. Ubiquitination is a post-translational modification that is widely present in cells to regulate the level of intracellular proteins, and is closely related to cancer progression. TRIM8 as an E3 ligase is one of the members of ubiquitination. In order to characterized the function of TRIM8 in lung adenocarcinoma, we overexpressed TRIM8 in different p53-type cell lines (A549, CL1-0 and H358)

2025-02-12 | GSE229282 | GEO

GAPDH inhibition in A549 and H358 lung cancer cells

Project description:Human lung cancer cell lines A549 and H358 were obtained from (Biobank of Medical University of Graz) and cultured in RPMI 1640 (R0883; Sigma) supplemented with 10% fetal bovine serum (FBS; Gibco), 5 mM glutamine and 5 mM Pen Step, and sub-cultured regularly. For siRNA mediated knock-down of GAPDH, 150,000 A549 and H358 cells were seeded in triplicates of a six-well plate and transfected upon reaching ca. 60% confluency with silencerTM siRNA kit targeting GAPDH or non-target control (AM4605; Thermo), using RNAiMax (Thermo) and according to the manufacturer’s instructions for 6-well plate scale. For GAPDH inhibition, 150.000 A549 and H358 cells were seeded in six replicates per condition, then treated with 10 µM koningic acid (KA) or vehicle control (dmso). 48 h post transfection or 24 h post KA treatment, cells were harvested in 500 µl of harvesting solution (80% methanol in 50 mM ammonium acetate with 2.5 mM N-ethylmaleimide) and processed according to one-pot redox approach.

2025-05-12 | PXD061610 | Pride

Expression data from CL1-0 and CL1-5 lung cancer cell line.

2012-12-11 | GSE42407 | GEO

Expression data from CL1-0 and CL1-5 lung cancer cell line.

Project description:A lung cancer cell model of invasive transformation was developed to select progressively invasive cell populations from a parental cell line of human lung adenocarcinoma, CL1. Five progressive sub-clones namely, CL1-1, CL1-2, CL1-3 CL1-4, and CL1-5 were selected using transwell and displayed increasing invasion potential (Chu et al, 1997). Here, we used microarrays to analyze and compare gene expression profiles between CL1-0 and CL1-5 for the identification of invasion/metastasis associated gene signatures. CL1-0 and CL1-5 lung cancer cell lines were used for RNA extraction and hybridization on Affymetrix microarrays. A total of 6 chips were used for microarray analysis including three biological repeats from CL1-0 and three biological repeats from CL1-5.

2012-12-11 | E-GEOD-42407 | biostudies-arrayexpress

Expression data from AK4 overexpression in CL1-0 lung cancer cell line and AK4 knockdown in CL1-5 lung cancer cell line

Project description:We demonstrate that AK4 down-regulation shRNAs significantly reduced cell migration and invasion in highly invasive lung cancer cell lines in vitro, as well as in lung metastases in vivo We used microarrays to analyze the AK4 regulated gene expression underlying invasion-metastasis cascade. CL1-0 lung adenocarcinoma cells with AK4 overexpression and CL1-5 cells with AK4 knockdown were selected for RNA extraction and hybridization on Affymetrix microarrays.

2012-12-03 | E-GEOD-37903 | biostudies-arrayexpress

RNA microarray was performed from lung adenocarcinoma cell CL1-0 and CL1-5 that were manipulated LCRMP-1 expression.

Project description:Transcriptomic profiling of CL1-0 and CL1-5 cells with altered LCRMP-1 expression revealed that LCRMP-1 promotes angiogenesis by regulating angiogenesis facotr transcription, implicating its role as a transcriptional co-regulator in lung cancer progression.

2025-10-02 | GSE308874 | GEO

Gene expression profiling data following TRIM8 knockdown in MCF-7 cells

Project description:Breast cancer (BC) is the most common female malignancies worldwide, and 70% of cases are estrogen receptor α (ERα) positive. In this study, we report that the E3 ubiquitin ligase TRIM8 acts as a novel regulator of ER signaling. TRIM8 is downregulated in BC and is associated with poor prognosis. In addition, the protein level of TRIM8 is negatively correlated with ERα expression. To investigate whether TRIM8 mediated estrogen signaling pathway, we generated a knockdown model of TRIM8 in human MCF7 cells.

2020-08-29 | GSE157109 | GEO

Human kinome CRISPR knockout screen in H358 parental and sotorasib resistant H358 cells

Project description:A human kinome CRISPR knockout screen in H358 parental and sotorasib-R H358 cells using Addgene pooled libraries (#75314).

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Transcriptomic profile of TRIM8-driven neural stem cells

Project description:We recently described TRIM8, a nuclear E3 ubiquitin ligase, whose expression inversely correlates with glioma grade. TRIM8 restoration suppresses cell growth and induces a significant reduction of clonogenic potential in both U87MG glioblastoma and patients’ primary glioma cell lines. Since E3 ubiquitin ligase proteins regulate carcinogenesis through the timely control of many cellular processes such as DNA damage response, metabolism, transcription, and apoptosis, we reasoned that TRIM8 activity might impact on cell transcriptome patterns, thereby promoting cancer development and progression. Therefore, we profiled the whole transcriptome of normal embryonic neural stem cells (eNSC) infected with a retrovirus expressing FLAG-Trim8 by using RNA-Seq. RNA-Seq revealed 1365 differentially expressed transcripts of 912 genes. 723 of them (corresponding to 648 RefSeq genes) differed significantly of at least 1.5 folds (192 upregulated transcripts of 178 genes and 531 downregulated transcripts of 470 genes). 80 genes, among all differentially expressed genes, resulted to significantly enrich 18 pathways by IPA analysis. 53% of these genes (43 out of 80 genes) are related to cell-morphology, cell death and survival, with a preponderantly representation of signaling pathways related to neurotransmission and to CNS, including axonal guidance, GABA Receptor, ephrin B, synaptic long-term potentiation/depression, and glutamate receptor. Specifically, our results substantiate the role of TRIM8 in the brain functions through the dysregulation of genes involved in different pathways, including JAK-STAT. Finally, we provided additional evidence about the existence of a functional interactive crosstalk between TRIM8 and STAT3 with possible implications in the development and progression of glioma.

2018-04-07 | GSE112810 | GEO

Transcription factor POU3F2 regulates TRIM8 expression contributing to cellular functions implicated in schizophrenia

Project description:Schizophrenia (SCZ) is a neuropsychiatric disorder with aberrant expression of multiple genes. However, identifying its exact causal genes remains a considerable challenge. The brain-specific transcription factor POU3F2 (POU domain, class 3, transcription factor 2) has been recognized as a risk factor for SCZ, but our understanding of its target genes and pathogenic mechanisms are still limited. Here we report that 42 SCZ-related genes are regulated by POU3F2 in knockdown and RNA sequencing experiments of human neural progenitor cells (NPCs). Among those SCZ-related genes, TRIM8 (Tripartite motif containing 8) is located in SCZ-associated genetic locus and aberrantly expressed in patients with SCZ. Luciferase reporter and electrophoretic mobility shift assays (EMSA) showed that POU3F2 induces TRIM8 expression by binding to the SCZ-associated SNP (single nucleotide polymorphism) rs5011218, which impacts POU3F2 binding efficiency at the promoter region of TRIM8. We investigated the cellular functions of POU3F2 and TRIM8 as they co-regulate several pathways related to neural development and synaptic function. Knocking down either POU3F2 or TRIM8 promoted the proliferation of NPCs, inhibited their neuronal differentiation, and impaired the excitatory synaptic transmission of NPC-derived neurons. These results indicate that POU3F2 regulates TRIM8 expression through the SCZ-associated SNP rs5011218, and both genes may be involved in the etiology of SCZ by regulating neural development and synaptic function.

2020-12-01 | GSE143692 | GEO

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