|
| Status |
Public on Nov 25, 2014 |
| Title |
B7_1 |
| Sample type |
RNA |
| |
|
| Source name |
MCF7
|
| Organism |
Homo sapiens |
| Characteristics |
cell line: MCF7 breast cancer cell line
treatment: HOXB7 overexpression
|
| Treatment protocol |
pcDNA3-Flag-HOXB7 or pcDNA3-Vector were stably transfected into MCF-7 cells using Lipofectamine 2000 (Invitrogen, Life Technologies, Carlsbad, California, United States).
|
| Growth protocol |
Cell lines were maintained at 37°C in a 5% CO2 incubator. MCF-7 cells and derivatives were cultured in DMEM medium (Mediatech, Manassas, Varginia) supplemented with 10% heat-inactivated FBS (Mediatech), 100 IU/mL penicillin, and 100 μg/mL streptomycin (GIBCO, Life Technologies, Carlsbad, California).
|
| Extracted molecule |
total RNA |
| Extraction protocol |
Total RNA was extracted with RNeasy Mini Kit (Qiagen)
|
| Label |
Biotin
|
| Label protocol |
Biotinylated cRNA were synthesized using Illumina TotalPrep RNA Amplification Kit (AMIL1791, Ambion, Austin, TX) following the standard protocol.
|
| |
|
| Hybridization protocol |
Standard Illumina hybridization protocol
|
| Scan protocol |
Standard Illumina scan protocol
|
| Description |
MCF7 cell-line over-expressing HOXB7
|
| Data processing |
Raw data was exported from Illumina GenomeStudio and imported into R using the lumi package. Data was normalized using lumi package from R statistical environment using the 'neqc' function (background subtraction, quantile normalization with control probes).
|
| |
|
| Submission date |
Nov 25, 2014 |
| Last update date |
Nov 25, 2014 |
| Contact name |
Saraswati Sukumar |
| E-mail(s) |
saras@jhmi.edu
|
| Phone |
410-614-2479
|
| Organization name |
Johns Hopkins School of Medicine
|
| Department |
Breast Cancer Program
|
| Lab |
Sukumar Lab
|
| Street address |
1650 Orleans St, CRB 1, Rm 132
|
| City |
Baltimore |
| State/province |
MD |
| ZIP/Postal code |
21231 |
| Country |
USA |
| |
|
| Platform ID |
GPL10558 |
| Series (1) |
| GSE63607 |
HOXB7 is an ERα cofactor in the activation of HER2 and multiple ER target genes leading to endocrine resistance |
|
