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Knockdown of EI24 in ZR-75-1 cells

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE52508 | GEO | 2013/11/20

SECONDARY ACCESSION(S): PRJNA229138

REPOSITORIES: GEO

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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

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ZR-75-1 microarray expression data

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Expression data from EI24 overexpression in ESCC cells

Project description:Analysis of EC109 cells following overexpression of EI24 and control vector. Etoposide induced 2.4 kb transcript (EI24), also known as p53-induced gene 8 (PIG8), is located on human chromosome 11q23. Serving as a p53 responsive pro-apoptotic factor, EI24 plays a pivotal role in inhibiting cell growth and activating autophagy and is associated with drug resistance. Results provide insight into the role of EI24 in cell proliferation and drug resistance of ESCC cells.

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Baseline Expression of Inflammatory Cytokines and Receptors in the ZR-75 Human Breast Cancer Cell Line

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Expression analysis of breast cancer cell lines SKBR-3 and ZR-75-1 upon treatment of LMO2 overexpression or knocking-down

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Homo sapiens

Project description:Knockdown of EI24 in ZR-75-1 cells

| PRJNA229138 | ENA

Estrogen priming of breast cancer ZR-75-1 cells results in a unique response to a timecourse of progesterone and medroxyprogesterone acetate exposure

Project description:A timecourse assessment of the response of ZR-75-1 breast cancer cells to progestogens in cells pretreated with estrogen. P4 treatment in cells pretreated with E2 results in a unique transcriptional response, including upregulation of ErbB growth factor pathways and alteration of the intrinsic subtype of the breast cancer cells.

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