biostudies-arrayexpressOleg Grinchuk V.Homo sapienshttps://www.ebi.ac.uk/biostudies/studies/E-MTAB-15849Through various approaches we demonstrate that SYCP1 is aberrantly re-expressed in tumor cells, where it actively promotes DNA damage repair, cell cycle progression, and malignant growth. SYCP1 binds chromatin at regulatory elements and directly controls transcriptional programs governing genome maintenance, including key effectors such as CCNB1, PCNA, RAD51C, and H2AX. Loss of SYCP1 impairs DNA repair kinetics, attenuates tumor cell proliferation and migration, and increases sensitivity to chemotherapeutics cisplatin and gemcitabine. Mechanistically, SYCP1 interfaces with chromatin remodeling complexes and transcription factors SP1 and SP2, modulating their genomic occupancy and facilitating oncogenic transcriptional outputs. Our findings illuminate a previously unrecognized moonlighting function of SYCP1 in somatic cancer cells and position it as a critical chromatin-associated regulator of genome stability. In the presented RNA-seq experiment, we aimed to identify the differentially expressed genes between samples of wild type MCF7 cells and the samples with CRISPR/Cas9-mediated SYCP1 gene KO.biostudies-arrayexpressLibrary Construction - At least 5x105 cells were lysed using Trizol reagent, and RNA was extracted with the Directzol™ RNA Mini Prep Kit (Zymo Research, cat. no. R2050) according to the manufacturer's protocol. 1 μg of RNA was used as input for library preparation. rRNA depletion was performed using the NEBNext rRNA Depletion Kit v2 (NEB, cat. no. E7405), followed by cDNA synthesis, end prep, and library amplification using the NEBNext Ultra II Directional RNA Library Prep Kit for 56 Illumina (NEB, cat. no. E7760). The average fragment length was determined using D1000 ScreenTape (Agilent, cat. no. 5067–5582) with D1000 reagents (Agilent, cat. no. 5067–5583), and sample concentration was measured with the Qubit 3.0 Fluorometer (Life Technologies). Next-generation sequencing was performed by Macrogen, SingaporeSequencing - Next-generation sequencing was performed by Macrogen, Singapore.Nucleic Acid Extraction - Upon bacterial transformation, colonies were selected for plasmid isolation using the ZymoPURE Plasmid Miniprep Kit (Zymo Research, cat. no. D4214) and subsequently subjected to Sanger sequencing to identify editing events.Growth Protocol - Cell lines were maintained in DMEM media supplemented with 2 mM l-glutamine (Invitrogen) and 10% (v/v) fetal calf serum (FCS) at 37 °C in 5% CO2. Cell lines were never maintained for more than 30 passages or 2 months of continuous culturing. Cell lines were tested for mycoplasma on a tri-monthly basis.Sample Treatment - SCYP1 knockout was generated through CRISPR/Cas9-mediated genome editing in MCF7 cells and was carried out by Synthego, using a guide RNA (gRNA) targeting exon 2 (5’ -AAGCAGCAGTCAGGTGTCTG-3’). Single clones were genotyped using Zero Blunt™ TOPO™ PCR Cloning Kit (Invitrogen, cat. no. 450245) according to the manufacturer’s instructions.OrganizationMINSEQE ScoreAssays and DataProcessed DataMAGE-TAB FilesSequence Alignment - RNA-seq data quality was monitored via FASTQC package (https://www.bioinformatics.babraham.ac.uk/projects/fastqc/).Reads preprocessing was performed by Trim Galore with default parameters.Mapping of RNA-seq reads was done using bowtie2 with default parameters for paired RNA-seq data. RSEM software (Li and Dewey, 2011) were used to quantify the gene-level expression.Data Transformation - TPM (transcript per million) normalization of raw counts was performed using Rsem software.UnknownTranscriptomicsGenomicsProteomicsIllumina HiSeq 4000RNA-seq of coding RNAHomo sapiensOleg Grinchuk V.falseEffect of CRISPR/Cas9-mediated SYCP1 gene expression depletion in MCF7 breast adenocarcinoma cells (RNA-seq)Through various approaches we demonstrate that SYCP1 is aberrantly re-expressed in tumor cells, where it actively promotes DNA damage repair, cell cycle progression, and malignant growth. SYCP1 binds chromatin at regulatory elements and directly controls transcriptional programs governing genome maintenance, including key effectors such as CCNB1, PCNA, RAD51C, and H2AX. Loss of SYCP1 impairs DNA repair kinetics, attenuates tumor cell proliferation and migration, and increases sensitivity to chemotherapeutics cisplatin and gemcitabine. Mechanistically, SYCP1 interfaces with chromatin remodeling complexes and transcription factors SP1 and SP2, modulating their genomic occupancy and facilitating oncogenic transcriptional outputs. Our findings illuminate a previously unrecognized moonlighting function of SYCP1 in somatic cancer cells and position it as a critical chromatin-associated regulator of genome stability. In the presented RNA-seq experiment, we aimed to identify the differentially expressed genes between samples of wild type MCF7 cells and the samples with CRISPR/Cas9-mediated SYCP1 gene KO.2026-03-15T00:00:00Z2026-03-15T02:04:33.575Z2025-10-24T15:22:57.306ZE-MTAB-15849ERP182989EFO_0002944EFO_0004170EFO_0003789EFO_0004917EFO_0003816EFO_0003738EFO_0004184EFO_0003969