{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown","Transcriptomics","Genomics","Proteomics"],"submitter":["Minji An"],"instrument_platform":["Agilent 2100 Bioanalyzer; Illumina TruSeq Stranded mRNA Prep Kit","CO₂ incubator (Thermo Fisher Scientific)","Illumina NovaSeq 6000","Illumina TruSeq Stranded mRNA Library Prep Kit","Biological safety cabinet (Thermo Fisher Scientific)","Lipofectamine RNAiMax transfection reagent (Invitrogen)"],"study_type":["RNA-seq of total RNA"],"organism":["Homo sapiens"],"species":["Homo sapiens"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16017"],"description":["This study aimed to investigate transcriptomic alterations induced by androgen receptor (AR) silencing in the radioresistant Hs578T triple-negative breast cancer (TNBC) cells. Using siRNA-mediated knockdown of AR, RNA sequencing was performed to identify genes and pathways associated with AR signaling in radioresistant TNBC cells. Comparative transcriptomic profiling between control and AR-silenced cells revealed significant changes in pathways related to DNA damage response, apoptosis, and mTOR signaling. These data provide insights into the molecular mechanisms underlying AR-mediated regulation in TNBC and potential targets for therapeutic intervention."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Sequencing - Sequencing was performed on the Illumina NovaSeq 6000 platform using paired-end reads. The resulting FASTQ files were processed with BBDuk for adapter trimming and quality filtering, aligned to the human GRCh38 (Ensembl v34) reference genome using STAR (v2.7.1a), and gene-level quantification was performed using RSEM (v1.3.1).","Growth Protocol - Hs578T parental and RR cells were cultured in Dulbecco’s Modified Eagle’s Medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 25 mM HEPES. Cells were maintained at 37 °C in a humidified atmosphere of 95% air and 5% CO₂.","Sample Collection - Hs578T parental and radioresistant (RR) cells were harvested 24 hours after transfection for RNA extraction. Cells were washed twice with cold PBS and collected directly from culture dishes using cell scrapers, ensuring consistent handling across all samples.","Nucleic Acid Extraction - Total RNA was extracted using the Illumina TruSeq Stranded mRNA Library Prep Kit (Illumina, San Diego, CA, USA) according to the manufacturer’s protocol. RNA integrity was verified using an Agilent 2100 Bioanalyzer before library preparation.","Sample Treatment - For gene knockdown experiments, cells were transfected with control siRNA (sc-37007) or AR siRNA (sc-29204) using Lipofectamine RNAiMax (Invitrogen, 13778-150) following the manufacturer’s instructions. siRNAs were diluted to a final concentration of 10 nM in Opti-MEM and incubated for 15 min with Lipofectamine RNAiMax at a 1:1 ratio before being added to the cells.","Library Construction - RNA-seq libraries were constructed using the Illumina TruSeq Stranded mRNA Library Prep Kit (Illumina, San Diego, CA, USA). Poly(A)+ mRNA was purified from total RNA, fragmented, and reverse transcribed to cDNA. After adapter ligation and PCR amplification, libraries were quantified and quality-checked prior to sequencing."],"figure_sub":["Organization","MINSEQE Score","Assays and Data","MAGE-TAB Files"],"pubmed_authors":["Minji An"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptomic profiling of AR knockdown in human triple-negative breast cancer Hs578T cells","description":"This study aimed to investigate transcriptomic alterations induced by androgen receptor (AR) silencing in the radioresistant Hs578T triple-negative breast cancer (TNBC) cells. Using siRNA-mediated knockdown of AR, RNA sequencing was performed to identify genes and pathways associated with AR signaling in radioresistant TNBC cells. Comparative transcriptomic profiling between control and AR-silenced cells revealed significant changes in pathways related to DNA damage response, apoptosis, and mTOR signaling. These data provide insights into the molecular mechanisms underlying AR-mediated regulation in TNBC and potential targets for therapeutic intervention.","dates":{"release":"2025-11-14T00:00:00Z","modification":"2025-11-14T02:02:00.763Z","creation":"2025-11-06T10:28:05.14Z"},"accession":"E-MTAB-16017","cross_references":{"ENA":["ERP183680"],"EFO":["EFO_0002944","EFO_0004170","EFO_0009653","EFO_0003789","EFO_0005518","EFO_0004184","EFO_0003969"]}}