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Expression data in H1299 after retinoblastoma binding protein-2 (RBP2) knockdown

ABSTRACT: To identify genes whose expression was affected by RBP2, we performed gene expression microarray analysis in control and RBP2 depletion human lung cancer cell line. Two individual shRNA (RBP2 KD1 and RBP2 KD2) were used to limit potential off-target effects. One scramble short haripin RNA (shRNA) and two individual shRNAs to the human RBP2 gene (RBP2 KD1 and RBP2 KD2) were used. Two replicates per group were used. H1299 cells were infected with lentivirus which carriy shRNAs for 3 days. RNA was isloated by Trizol reagent and analyzed by bioanalyzer. Microarray experiments was performed by the Affymetrix Gene Expression Service Laboratory at Academia Sinica.

ORGANISM(S): Homo sapiens

SUBMITTER: Feng-Mao Lin

PROVIDER: E-GEOD-41443 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Histone demethylase RBP2 promotes lung tumorigenesis and cancer metastasis.

Teng Yu-Ching YC Lee Cheng-Feng CF Li Ying-Shiuan YS Chen Yi-Ren YR Hsiao Pei-Wen PW Chan Meng-Yu MY Lin Feng-Mao FM Huang Hsien-Da HD Chen Yen-Ting YT Jeng Yung-Ming YM Hsu Chih-Hung CH Yan Qin Q Tsai Ming-Daw MD Juan Li-Jung LJ

Cancer research 20130530 15

The retinoblastoma binding protein RBP2 (KDM5A) is a histone demethylase that promotes gastric cancer cell growth and is enriched in drug-resistant lung cancer cells. In tumor-prone mice lacking the tumor suppressor gene RB or MEN1, genetic ablation of RBP2 can suppress tumor initiation, but the pathogenic breadth and mechanistic aspects of this effect relative to human tumors have not been defined. Here, we approached this question in the context of lung cancer. RBP2 was overexpressed in human ...[more]

PMID: 23722541

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Expression data in H1299 after retinoblastoma binding protein-2 (RBP2) knockdown

Project description:To identify genes whose expression was affected by RBP2, we performed gene expression microarray analysis in control and RBP2 depletion human lung cancer cell line. Two individual shRNA (RBP2 KD1 and RBP2 KD2) were used to limit potential off-target effects.

2013-06-20 | GSE41443 | GEO

Transcriptome alteration upon ZNF281 depletion in HCC cells

Project description:To find potential target gene of ZNF281 in HCC cells, the transcriptome analyse (RNA-seq) were performed in HLE HCC cell lines with or with ZNF281 depletion using shRNAs in lentivirus vectors Zinc finger protein 281 (ZNF281) has been implicated in the progression of several types of cancer. However, its functionality and transcriptional targets in hepatocellular carcinoma (HCC) remains elusive. In the present study, we discovered that the expression of ZNF281 was increased in tumor tissues and cell lines, and positively correlated with vessel invasion in HCC. We took RNA interference approach and constructed 2 shRNAs lentivirus vectors targeting different regions of ZNF281 which were named as ZNF281.kd1 and ZNF281.kd2 respectively. Knockdown of ZNF281 suppressed proliferation, migration and invasion of HCC cells. In searching for novel ZNF281 regulated genes, RNA-seq was performed on BGI-seq500 platform using the obtained stable cells of Con, ZNF281.kd1 and ZNF281.kd2 in HLE background (each in duplicate). The criteria of log2 FC (fold change) >1.5, and q value <0.001 was set for calling differentially expressed genes (DEGs). Besides, to minimize the off-target effect of single shRNAs, only DEGs that show consistent trend of alteration (up-regulated or down-regulated in both ZNF281.kd1 and ZNF281.kd2 groups against control shRNA group) were selected as potential ZNF281 targets. A list of potential targets was identified, including both up-regulated and down-regulated genes upon ZNF281 depletion. Further mechanistic studies were performed to uncover transcriptional regulation of ZNF281 on these genes. Our study was supposed to be helpful for understanding the molecular mechanism underpinning progression of HCC, and might also hold therapeutic potential for HCC treatment.

2020-03-07 | GSE146496 | GEO

RNA-seq of mouse embryonic stem cells with altered Zfp207 expression

Project description:We have observed the transcriptomic differences between mouse embryonic stem cells transfected with lentiviral scramble shRNA (SC) and with lentiviral Zfp207 shRNA (two different constructions, KD1 and KD2)

2021-03-31 | E-MTAB-10108 | biostudies-arrayexpress

HSL119 results in gene expression changes equivalent to HUNK shRNA

Project description:The goal of this study was to determine the gene similarities and overlap between human HER2+ breast cancer cells treated with a HUNK inhibitor (HSL119) and samples engineered with HUNK shRNA (KD1 and KD2). A main objective was to determine if genes related to the AKT pathway were changed in HUNK treated or HUNK knockdown groups compared to control.

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Functional and Mechanistic Studies of XPC DNA-Repair Complex as Transcriptional Coactivator in Embryonic Stem Cells

Project description:We recently identified the DNA repair complex XPC-RAD23B-CETN2 as a stem cell coactivator (SCC) required for OCT4 and SOX2 transcriptional activation. Here we investigate genome-wide the role of SCC in murine ESCs by mapping regions bound by its RAD23B subunit in wild type and Xpc-/- ESCs, and analyzing transcriptional profiles of SCC-depleted ESCs. RAD23B ChIP-seq in wild type murine ESCs was performed in two replicates; normal IgG were used as controls. RAD23B ChIP-seq in Xpc-/- mESCs was compared to normal IgG. Antibodies to immunoprecipitate RAD23B were raised in guinea pigs against the 108-177 peptide of murine RAD23B protein (NP_033037). Anti-sera were affinity-purified. For RNA-seq, we compared wild type JM8.N4 cells with either Rad23b-/- cells, Rad23b-/-Xpc KD1 or Rad23b-/-Xpc KD2 cells. Xpc was knocked down with two independent shRNAs (KD1 and KD2).

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Analysis of small EV proteomes reveals unique functional protein networks regulated by VAP-A

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2023-11-10 | PXD043796 | Pride

Empty-vector control and transgenic 35S-PaWRKY1 Arabidopsis

Project description:Transcriptional profiling of genes regulated by PaWRKY1 transcription factor A PaWRKY transcription factor from orchid plants is expressed in Arabidopsis, and the PaWRKY-regulated genes are studied Comparison of empty-vector control and transgenic 35S-PaWRKY1 Arabidopsis Affymetrix GeneChip assay were performed by the Affymetrix Gene Expression Service Lab (http://ipmb.sinica.edu.tw/affy/), supported by Academia Sinica, Taiwan

2010-07-07 | E-GEOD-22766 | biostudies-arrayexpress

Transcription profiling by high throughput sequencing of HNRNPC knockdown and control HeLa cells

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2013-01-31 | E-MTAB-1147 | biostudies-arrayexpress

Sriram2007_CellCycle

Project description:The model reproduces the time profile of species depicted in Figure 12a and 12 b. The authors communicated to the curator that there is a typo in the paper, the values of kd1 and kd2 are reversed. Model successfully reproduced using MathSBML.

2024-09-02 | BIOMD0000000181 | BioModels

CRTAC1 Enhances the Chemosensitivity of Non-Small Cell Lung Cancer to Cisplatin by Eliciting RyR-mediated Calcium Release and Inhibiting Akt1 Expression

Project description:Sensitivity to platinum-based combination chemotherapy is associated with a favorable prognosis in the patients of non-small cell lung cancer (NSCLC). Here, our results obtained from analyses of the Gene Expression Omnibus database of NSCLC patients showed that cartilage acidic protein 1 (CRTAC1) plays a role in the response to platinum-based chemotherapy. Overexpression of CRTAC1 increased sensitivity to cisplatin in vitro, whereas knockdown of CRTAC1 decreased chemosensitivity of NSCLC cells. In vivo mouse experiments showed that CRTAC1 overexpression increased the antitumor effects of cisplatin. CRTAC1 overexpression promoted NFAT transcriptional activation by increasing intracellular Ca2+ levels, thereby inducing its regulated STUB1 mRNA transcription and protein expression, accelerating Akt1 protein degradation, and in turn enhancing cisplatin-induced apoptosis. Taken together, the present results indicate that CRTAC1 overexpression increases the chemosensitivity of NSCLC to cisplatin treatment by inducing Ca2+-dependent Akt1 degradation and apoptosis, suggesting the potential of CRTAC1 as a biomarker for predicting cisplatin chemosensitivity. Our results further reveal that modulating the expression of CRTAC1 could be a new strategy for increasing the efficacy of cisplatin in chemotherapy of NSCLC patients.

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