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The p53 Target Gene Siva Enables Tumorigenesis

ABSTRACT: Siva is a p53target gene essential for p53-dependent apoptosis, although it can also promote proliferation through inhibition of p53 in some settings. Thus, the role of Siva in tumorigenesis remains unclear. Surprisingly, we find that Siva loss inhibits non-small cell lung cancer (NSCLC) development, suggesting that Siva facilitates tumorigenesis. Similarly, Siva knockdown in mouse and human NSCLC cell lines decreases proliferation and transformation. To gain an understanding of the molecular basis for the reduced proliferation and transformation resulting from Siva knockdown, we performed gene expression profiling experiments on LSZ4 and LSZ2 cells after Siva knockdown by lentiviral transduction with each of the two previously characterized shRNAs (shSiva1 and shSiva2) and each of two control shRNAs (shLacZ and shGFP). Hierarchical clustering revealed a notable difference in gene expression profiles between Siva knockdown and control samples. Differentially expressed genes were analyzed for enrichment in Gene Ontology (GO) terms using GeneSpring Analysis. We found that the most enriched GO terms included immune regulation – consistent with Siva’s known role in regulating NFкB signaling – as well as cell migration and metabolic processes.

ORGANISM(S): Mus musculus

PROVIDER: GSE66126 | GEO | 2015/05/15

SECONDARY ACCESSION(S): PRJNA275929

REPOSITORIES: GEO

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The p53 Target Gene Siva Enables Tumorigenesis

Project description:Siva is a p53target gene essential for p53-dependent apoptosis, although it can also promote proliferation through inhibition of p53 in some settings. Thus, the role of Siva in tumorigenesis remains unclear. Surprisingly, we find that Siva loss inhibits non-small cell lung cancer (NSCLC) development, suggesting that Siva facilitates tumorigenesis. Similarly, Siva knockdown in mouse and human NSCLC cell lines decreases proliferation and transformation. To gain an understanding of the molecular basis for the reduced proliferation and transformation resulting from Siva knockdown, we performed gene expression profiling experiments on LSZ4 and LSZ2 cells after Siva knockdown by lentiviral transduction with each of the two previously characterized shRNAs (shSiva1 and shSiva2) and each of two control shRNAs (shLacZ and shGFP). Hierarchical clustering revealed a notable difference in gene expression profiles between Siva knockdown and control samples. Differentially expressed genes were analyzed for enrichment in Gene Ontology (GO) terms using GeneSpring Analysis. We found that the most enriched GO terms included immune regulation – consistent with Siva’s known role in regulating NFкB signaling – as well as cell migration and metabolic processes. RNA from LSZ2 and LSZ4 non small cell lung cancer cells expressing control (shGFP1, shLacz) or Siva (shSiva1, shSiva2) hairpins was used. A total of seven control samples and eight test samples using different cell lines and hairpins were used.

2015-05-15 | E-GEOD-66126 | biostudies-arrayexpress

Identification of SAT1 regulated genes in GBM cells by microarray

Project description:We aimed to identify SAT1 regulated genes in U87MG cell by knockdown of SAT1 with two different shRNAs, and then compared knockdown cells to control cells with shGFP

2021-06-23 | GSE116395 | GEO

Knockdown of MRPL35 promotes cell apoptosis and inhibits cell proliferation in non-small-cell lung cancer

Project description:Background: Non-small cell lung cancer (NSCLC) is a major pathological type of lung cancer. However, its pathogenesis remains largely unclear. MRPL35 is a regulatory subunit of the mitoribosome, which can regulate the assembly of cytochrome c oxidases and play an important role in the occurrence of NSCLC. Methods:The expression of MRPL35 in NSCLC was detected by tissue microarray and immunohistochemistry. H1299 cells were infected with lentivirus to knockdown MRPL35, and the cells were subjected to crystal violet staining to assess the results of colony formation assays. A549 cells were infected by lentiviral particles-expressing shMRPL35 or shControl, and then subcutaneously injected into nude mice. Tumorigenesis in mice was detected by in vivo imaging. The potential pathway of MRPL35 in NSCLC was assessed by Western blotting. Results:MRPL35 was over-expressed in NSCLC tissue compared to para-cancerous and normal tissues. Knockdown of MRPL35 suppressed cell proliferation and decreased NSCLC progression both in vitro and in vivo. The possible molecular mechanisms were also clarified, which indicated that MRPL35 could be involved in cell apoptosis and proliferation by modulating the expression levels of CDK1, BIRC5, CHEK1, STMN1 and MCM2. Knockdown of MRPL35 activated p53 signaling pathway and inhibited cell cycle regulation. Conclusions:The oncogenic role of MRPL35 in NSCLC was potentially mediated through the cell cycle regulatory genes such as BIRC5, STMN1, CDK1, CHEK1 and MCM2, as well as activation of P53 signaling pathway.

2023-05-03 | GSE225959 | GEO

Gene expression profiles upon knocking down Cops2 or Cops5 in mouse embryonic stem cells

Project description:To understand the role of Cops2 in mouse embryonic stem cells, we applied expression microarray analysis with GFP knockdown, Cops2 knockdown (2 different hairpins), and Cops5 knockdown mouse ESCs. Mouse ESCs were transfected with shGFP, shCops2(two different shRNAs), or shCops5 plasmids. 72 hours after transfection, cells were harvested for RNA prep and microarray analysis.

2016-05-17 | E-GEOD-72436 | biostudies-arrayexpress

A novel USP9X substrate TTK contributes to tumorigenesis in non-small cell lung cancer

Project description:The X-linked deubiquitinase, USP9X, is implicated in multiple cancers by targeting various substrates. Increased expression of USP9X is observed in non-small cell lung cancer (NSCLC) and is correlated with poor prognosis. However, the molecular mechanism for USP9X regulating tumor cell survival and tumorigenesis in NSCLC is less defined. In this study, chemical labeling quantitative proteomic screening was applied to analyze A549 cells with or without USP9X RNA interference, and the resulting data suggested that TTK is a potential substrate of USP9X. Further experimental evidences confirmed that USP9X stabilized TTK via direct interaction and deubiquitination of TTK. Moreover, knockdown of USP9X or TTK inhibited cell proliferation, migration and tumorigenesis, and the immunohistochemical analysis of clinical NSCLC samples showed that the protein expression levels of USP9X and TTK were significantly elevated and positively correlated in tumor tissues. In summary, our data demonstrated that the USP9X-TTK axis may play a critical role in NSCLC, and could be considered as the potential therapeutic target.

2018-05-07 | PXD007726 | Pride

RNA-Seq analysis of prostate cancer cell line C4-2 treated with siRNA control (siCont), siEAF2, sip53 or concurrent siEAF2 and sip53

Project description:The tumor suppressor genes EAF2 and p53 are frequently dysregulated in prostate cancers. Recently, we reported that concurrent p53 nuclear staining and EAF2 downregulation were associated with high Gleason score. Combined loss of EAF2 and p53 in a murine model induced prostate tumors, and concurrent knockdown of EAF2 and p53 in prostate cancer cells enhanced proliferation and migration, further suggesting that EAF2 and p53 could functionally interact in the suppression of prostate tumorigenesis. Here, RNA-seq analyses identified differentially regulated genes in response to concurrent knockdown of p53 and EAF2. Several of these genes were associated with the STAT3 signaling pathway, and this was verified by significantly increased p-STAT3 immunostaining in the Eaf2-/-p53-/- mouse prostate. STAT3 knockdown abrogated the stimulation of C4-2 cell proliferation by concurrent knockdown of EAF2 and p53. Furthermore, immunostaining of p-STAT3 was increased in human prostate cancer specimens with EAF2 downregulation and/or p53 nuclear staining. Our findings suggest that simultaneous inactivation of EAF2 and p53 can act to activate STAT3 and drive prostate tumorigenesis.

2018-04-25 | GSE104729 | GEO

Knockdown of EI24 in ZR-75-1 cells

Project description:Analysis of ZR-75-1 cells folowing knockdown of EI24 (P53-Induced Gene 8) and control vector. As a p53 response gene, EI24 is known to controlling cell growth, apoptosis, and autophagy. Results provide insight into the role of EI24 in epithelial-to-mesenchymal Parental ZR-75-1 cells, ZR-75-1 cells with shGFP knockdown (control), Two independent clone of knockdown of EI24 in ZR-75-1. All samples are perfomed in duplicate. Total 8 samples exist.

2013-11-20 | E-GEOD-52508 | biostudies-arrayexpress

Comparison of gene expression in control and BRG1-knockdown H358 cell lines

Project description:Transcription was assessed in the human H358 NSCLC cell line after knockdown of BRG1, one of the mutually exclusive subunits of the SWI/SNF chromatin remodeling complex, by 2 different shRNAs.

2014-09-23 | GSE58542 | GEO

Comparison of gene expression in control and BRG1-knockdown H358 cell lines

2014-09-23 | E-GEOD-58542 | biostudies-arrayexpress

Glycine decarboxylase is a metabolic oncogene critical for tumor initiating cells and tumorigenesis in lung cancer

Project description:New approaches to cancer therapies could benefit from a better understanding of the molecular determinants critical to tumor initiating cells (TICs). Here we show that the metabolic enzyme glycine decarboxylase (GLDC) is critical for TICs in non-small cell lung cancer (NSCLC). From a broad range of primary NSCLC tumors, we isolated CD166+ lung TICs that consistently initiated tumorigenesis in NOD/SCID Il2rγ-/- mice. Lung TICs express high levels of the oncogenic stem cell factor LIN28B and the metabolic enzyme GLDC. Over-expression of GLDC and other glycine/serine metabolism enzymes, but not catalytically inactive GLDC, promotes cellular transformation and tumorigenesis. Metabolomic analysis found that GLDC induces dramatic changes in glycolysis and glycine/serine metabolism, leading to changes in pyrimidine metabolism to regulate cancer cell proliferation. Clinically, GLDC over-expression, observed in multiple cancer types, predicts poorer survival in lung cancer patients. Our findings establish a novel link between glycine metabolism and tumorigenesis, and provide novel targets for advancing anti-cancer therapy. Total RNA obtained from tumor sphere compared to CD166+ and CD166- selected cells of xenograft, primary tumor and normal donors

2011-10-25 | E-GEOD-33198 | biostudies-arrayexpress

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