{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"submitter":["Delamotte Pierre"],"organism":["Drosophila melanogaster"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16147"],"description":["Patient’s social environment might influence cancer outcome. This potentially happens in Drosophila, as we previously reported that the social context influences the growth of intestinal tumors. To uncover the underlying social-induced physiological mechanisms, we performed RNA-seq of isogenized beheaded tumorous Drosophila. Importantly, expression of several immune peptides varied according to the social-induced tumor growth effect. Furthermore, ectopic expression in tumors of the apoptotic-inhibitor p35 suppressed the social-induced effect. Next, we challenged the immune peptide Defensin, previously reported to suppress imaginal disc tumor growth through a cell-death/JNK-dependent network. Nonetheless, the social-induced tumor suppression was maintained upon Defensin overexpression or JNKK-knockdown in tumors, and in defensin mutants. Surprisingly, tumor growth was reduced in the latter, indicating that Defensin sustains the growth of these intestinal tumors. In summary, our study indicates that the social context affects the immune response and that a given immune peptide may have opposite effects depending on tumor type."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Nucleic Acid Extraction - RNA extraction from bodies was performed as described for heads (AKIKI et al. 2024). Briefly, RNAs were extracted using Trizol-chloroform and libraries for Illumina sequencing were prepared using the Illumina TruSeq total RNA stranded kit (GARRIDO et al. 2015) and sequenced using a NextSeq 550 instrument.","Library Construction - Analysis type: HISAT2 Reference genome: dmel-all-chromosome-r6.42.fasta (from FlyBase)","Sample Collection - For each replicate, groups of 100 tumorous flies were beheaded on dry ice; heads and bodies were store separately at -80°C. These flies were selected 10 days post tumor induction, as we assumed that the social-induced effect occur along the entire process of tumor growth.","Sequencing - DNA reads were converted into raw data (FASTQ files) and preprocessed to remove adapters, low-quality sequences and artefacts. Cleaned sequences were aligned to the reference genome \\\"dmel-all-chromosome-r6.42.fasta\\\" using HISAT2. Instrument name: NextSeq Instrument version: NS500446 Number of sequencing cycles: 75 (single end) Sample preparation protocol: Total RNA stranded Sequencing kit: NextSeq 500/550 High Output Kit v2 (75 cycles) Data Analysis Pipeline: HISAT2 (mapping) Run code: 211123","Sample Treatment - To generate tumors, females from line 1 or its derivative recombined to the defsk3 mutation were crossed to males from line 2 or its recombined derivatives. In their progeny non-balanced virgin females were selected and heat-shocked at 37°C for 1h15mins, two to three days after adult eclosion as previously detailed (DELAMOTTE et al. 2025). Fly groups were established immediately after heat-shock and maintained in a 25°C incubator on our standard media (GARRIDO et al. 2015), changed twice a week into new vials.","Growth Protocol - The yw,HS-flp;esg-gal4,UAS-GFP; FRT82B,Tub-Gal80 (line 1)  and w,HS-flp;UAS-RasV12;FRT82B,Apc2N175K,ApcQ8 (line 2)  stocks (MARTORELL et al. 2014) were maintained with co-segregating SM5-TM6B balancers. Prior to experiments, these lines were isogenized on chromosomes I, II and III from individual males crossed to a FM7; SM5-TM6B stock. Next, the UAS-RasV12 chromosome II from line 2 was recombined with either UAS-p35 (BDSC#5072), UAS-JNKK-RNAi (VDRC#109277), UAS-Defensin or the defsk3 mutant allele (PARVY et al. 2019), the latter being also recombined with the esg-gal4,UAS-GFP chromosome II from line 1; these recombined chromosomes were re-introduced into the parental lines. Control w1118 flies were used as healthy females in H-groups."],"figure_sub":["Organization","MINSEQE Score","Assays and Data","MAGE-TAB Files"],"data_protocol":["Data Transformation - Differential analyses between replicates were performed using the DESeq2 tool to identify genes whose expression significantly differs between experimental conditions. Output of DeSeq2 was finally analyzed with in-house Python scripts. The gene set enrichment analysis was performed using FlyEnrichr (CHEN et al. 2013; KULESHOV et al. 2016).","Sequence Alignment - See above with technical details. Additional material including MD5 matrixes have been added among the files."],"omics_type":["Unknown","Transcriptomics","Genomics","Proteomics"],"instrument_platform":["NextSeq 550"],"study_type":["RNA-seq of coding RNA"],"species":["Drosophila melanogaster"],"pubmed_authors":["Delamotte Pierre"],"additional_accession":[]},"is_claimable":false,"name":"Drosophila Sociality Influences Immune Peptide Load and Apoptosis-induced Tumor Suppression independently of the Antitumor Peptide Defensin","description":"Patient’s social environment might influence cancer outcome. This potentially happens in Drosophila, as we previously reported that the social context influences the growth of intestinal tumors. To uncover the underlying social-induced physiological mechanisms, we performed RNA-seq of isogenized beheaded tumorous Drosophila. Importantly, expression of several immune peptides varied according to the social-induced tumor growth effect. Furthermore, ectopic expression in tumors of the apoptotic-inhibitor p35 suppressed the social-induced effect. Next, we challenged the immune peptide Defensin, previously reported to suppress imaginal disc tumor growth through a cell-death/JNK-dependent network. Nonetheless, the social-induced tumor suppression was maintained upon Defensin overexpression or JNKK-knockdown in tumors, and in defensin mutants. Surprisingly, tumor growth was reduced in the latter, indicating that Defensin sustains the growth of these intestinal tumors. In summary, our study indicates that the social context affects the immune response and that a given immune peptide may have opposite effects depending on tumor type.","dates":{"release":"2026-01-01T00:00:00Z","modification":"2026-01-02T02:03:13.244Z","creation":"2025-11-17T10:49:54.385Z"},"accession":"E-MTAB-16147","cross_references":{"ENA":["ERP185153"],"EFO":["EFO_0002944","EFO_0004170","EFO_0003789","EFO_0004917","EFO_0005518","EFO_0003816","EFO_0003738","EFO_0004184","EFO_0003969"]}}