Project description:The study aims to elucidate the effect of histone methyltransferase SMYD3 on gene expression in MCF-7 breast cancer cell line. Knockdown luciferase control v.s. knockdown SMYD3 in MCF-7 breast cancer cell line were conducted. Results identify a large proportion of cell cycle-related genes regulated by SMYD3.
Project description:There are 64 replication-dependent histone genes with different isotypes associated with each class of the five histone types, H1, H2a, H2b, H3 and H4 in the human genome. In a previous report, we have showed that HIST1H2ac serves as a master regulator of ERalpha-dependent gene activation via ERalpha recruitment, and mediates chromatin looping of regulatory elements of estrogen receptor-targeted genes. Here, we performed whole genome bisulfite sequencing of MCF-7 upon suppressing H2ac expression through siRNA transfection using two different siRNAs to determine the knockdown effect on DNA methylation. Our analysis showed the DNA methylation of ~99% of the genome were mostly unchanged comparing to normal MCF-7 (methylation levels difference within 0.2).
Project description:The breast cancer cell line MCF-7 was engineered to overexpress the Twist gene resulting in the MCF-7/Twist cell line. To study which miRNA are regulated by Twist, we employed whole genome microarray expression profiling and compared miRNA expression between MCF-7/Twist and MCF-7 cells.
Project description:We show that most binding events of NR2F2 occur together with the ERα binding sites.To address the functional relationship between NR2F2 and ERα, we assessed the role of NR2F2 in oestrogen-induced growth in ER positive cell line MCF-7. The MTT experiment showed that inhibition of NR2F2 prevented the oestrogen-induced proliferation of MCF-7 cells.To further explore the effect of NR2F2 on estrogen response, We expanded our knockdown studies by performing RNA-seq analysis for MCF-7 cells transfected with control or NR2F2 shRNAs with or without E2.
Project description:To measure the levels of expression of retrotransposon individual copies, and particularly of LINE-1 (L1) elements of the L1HS-Ta subfamily, we performed 2x150 bp paired-end and strand-specific RNA-seq on polyA+ RNA of MCF-7 and 2102Ep cells, which express high levels of L1. To confirm the origin of the L1-specific signal, we also performed RNA-seq upon shRNA-mediated L1 knockdown. sh960 relates to a scramble shRNA control. sh1083 and sh1085 relate to two distinct shRNAs directed against the ORF1 region of L1.3 (GenBank L19088) as a prototype L1HS-Ta.
Project description:To explore elements contributing to radioresistance in breast cancer, we established radioresistant human breast cancer cell line MCF-7.
Project description:The telomeric amplicon at 8p12 is common in ER+ breast cancers. Array-CGH and expression analyses of 1172 tumors revealed ZNF703/Zeppo1 was the single gene within the minimal amplicon and was amplified predominantly in the Luminal B subtype. Amplification was shown to correlate with increased gene and protein expression and was associated with a distinct expression signature and poor outcome. In the luminal MCF-7 cell line manipulation of ZNF703 expression altered transcription of genes also present within the primary tumor signature, including TGFBR2 (whose promoter was bound by ZNF703). Overexpression of ZNF703 rendered MCF-7 cells insensitive to TGFβ-induced suppression of mammosphere formation. Forced overexpression of ZNF703 in normal human breast epithelial cells enhanced the frequency of in vitro colony-forming cells from luminal progenitors. Together these data strongly point to ZNF703/Zeppo1 as a novel oncogene in Luminal B breast cancer.