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Gene expression profiling of Ctr9-regulated transcriptome in ER?-positive breast cancer.

ABSTRACT: Ctr9, the key scaffold subunit in human RNA polymerase II associated factor complex (PAFc), has diverse functions in cells and has been implicated in human diseases. Recently, our study found that loss of Ctr9 led to apparent morphological change, decrease of proliferation, and reduced colony formation in ER?(+) breast cancer cells. Moreover, Ctr9 and ER? show positive correlation at protein levels and the high levels of Ctr9 are associated with poor survival among all women with ER?(+) breast cancers, and specifically among those treated with tamoxifen. To gain a molecular understanding of the role of Ctr9 in promoting ER?(+) breast cancer, we performed a microarray gene expression profiling of Ctr9-regulated transcriptome. Here we provide the experimental details and analysis of the microarray data, which have been deposited into Gene Expression Omnibus (GEO): GSE73388.

SUBMITTER: Zeng H

PROVIDER: S-EPMC4778656 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature

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Gene expression profiling of Ctr9-regulated transcriptome in ERα-positive breast cancer.

Zeng Hao H Xu Wei W

Genomics data 20151217

Ctr9, the key scaffold subunit in human RNA polymerase II associated factor complex (PAFc), has diverse functions in cells and has been implicated in human diseases. Recently, our study found that loss of Ctr9 led to apparent morphological change, decrease of proliferation, and reduced colony formation in ERα(+) breast cancer cells. Moreover, Ctr9 and ERα show positive correlation at protein levels and the high levels of Ctr9 are associated with poor survival among all women with ERα(+) breast c ...[more]

PMID: 26981377

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Project description:Objective:Regulator of chromosome condensation 2 (RCC2) has been reported to be involved in the regulation of cell cleavage. This study investigated the effect of RCC2 expression on breast tumorigenesis. Methods:MCF-7 cells originating from estrogen receptor-positive (ER+) breast cancer were transfected with anti-RCC2 siRNA or RCC2-expressing plasmids. Cell proliferation, apoptosis, migration, and cytokine production in the transfected cells were examined using the CCK-8 assay, wound healing assay, and flow cytometry, respectively. PCR array was used to investigate the tumorigenic pathway of RCC2 in MCF-7 cells transfected with the anti-RCC2 siRNA. MCF-7 cells were also transfected with lentivirus-containing anti-RCC2 short hairpin RNA and were injected into BALB/c nude mice to generate tumor-bearing mice. Tumor growth in the mouse model was examined using magnetic resonance imaging by diffusion-weighted imaging analysis. Results:Western blotting and immunohistochemistry detected significantly increased expression of RCC2 in ER?+?breast tumor tissues compared with breast fibroadenoma samples. Inhibiting RCC2 expression decreased cell migration and stimulated apoptosis in MCF-7 cells, while overexpressing RCC2 stimulated cell migration and inhibited apoptosis. The inhibition of RCC2 expression significantly decreased breast tumor growth and IL-6 levels in the tumor-bearing mice. PCR array demonstrated that inhibiting RCC2 expression significantly decreased the expression of IGF1 and TWIST1, two well-known tumor-enhancing genes, in MCF-7 cells; conversely, overexpressing RCC2 increased the expression levels of these two genes in the transfected cells. This result was verified in the mouse model following inhibition of RCC2 expression in MCF-7 cells. Additionally, estradiol-17? suppressed MCF-7 cell apoptosis, stimulated cell proliferation and cell migration, and increased RCC2, IGF1, and TWIST1 expression. The siRNA-mediated inhibition of RCC2 expression alleviated the inhibitory effects of estrogen on apoptosis in MCF-7 cells, while overexpressing RCC2 enhanced the estrogen-driven inhibition of apoptosis. Modifying RCC2 expression had no impact on MCF-7 cell proliferation in the presence or absence of estradiol-17?. Conclusions:Our results suggest that estrogen-induced RCC2 expression prompts IGF1, TWIST1, and IL-6 expression, stimulates cell migration, and inhibits apoptosis to contribute to ER?+?breast tumorigenesis.

Dataset Information

Gene expression profiling of Ctr9-regulated transcriptome in ER?-positive breast cancer.

Publications

Gene expression profiling of Ctr9-regulated transcriptome in ERα-positive breast cancer.

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