Project description:Cancer development is complicated, it invloves a series of gene expression change. As demonstrated in several reports, HP1γ is upregulated in some types of cancer, and it is essential for cancer development.We want to further clarify HP1γ function in bladder cancer. We used microarrays to determine the gene expression profile in bladder cancer cell line T24 with depletion of HP1γ.
Project description:Cbx3 (HP1γ) that is a member of the heterochromatin protein 1 family play important roles in development and differentiation. To determine the regulatroy mechanisms of Cbx3 during neural differentiation from ESCs to NPCs, we performed RNA-seq analysis of ESCs or ESC-derived NPCs depleted for Cbx3 or Cbx3-assocatied Mediator subunit Med26.
Project description:Cbx3 (HP1γ) that is a member of the heterochromatin protein 1 familiy enriched in gene bodies of pluripotent ESCs but promoters of differentiated pre-iPSCs. To determine whether Cbx3 becomes enriched at promoters to influence gene regulation during differentiation, we converted ESCs to NPCs in monolayer culuture and performed genomewide ChIP-seq of Cbx3. Our results shows that Cbx3 enriches at the promoters of genes upon differentiation of ESCs to NPCs and stablizes the binding of Mediator subunit Med26 to pre-initiation complex (PIC) in NPCs.
Project description:Purpose: To investigate the tumor-promoting role of STIL in bladder cancer. Method: We established the STIL knockout cell line in which the target gene was knocked out by sgRNA. RNA was extracted from cells using trizol reagent(Invitrogen) Result: Through RNA-sequencing analysis of wild-type and STIL-deficient UMUC3 cell lines, the downstream signaling pathways that STIL may be involved in were determined. We found that the PI3K/AKT/mTOR signaling pathway and c-myc were significantly inactivated when STIL was knocked out in bladder cancer. Our RNA-sequencing analysis results showed that the downstream molecules of c-myc (MCM4, HSPD1, EIF2S2, DDX21, DDX18, CBX3, ABCE1) were significantly down-regulated in bladder cancer cells after knockout. Conclusion: STIL enhances the PI3K/AKT/mTOR pathway, which consequently upgraded the expression of c-myc, ultimately promoting the occurrence and progression of bladder cancer C. STIL may suggest potential utility for bladder cancer therapy.
Project description:Temporal and spatial regulation of trimethylation of histone H3 lysine27 (H3K27me3) is crucial for cell lineage commitment and development. Resetting the ground state of H3K27me3 is important for establishing a proper development program of primordial germ cells (PGCs). The mechanisms that regulate global erasure of epigenetic information in the germ line are not well understood. Here we show that HP1γ suppresses the demethylation activity of Utx through direct interaction in vitro and in vivo. Down-regulation of mammalian heterochromatin protein 1 gamma (HP1γ) coincides with transient loss of H3K27me3 in PGCs on Embryonic Day 10.5 (E10.5). Furthermore, transient abolishment of HP1γ promotes the induction of embryonic stem cells into putative PGCs in vitro. These data reveal a cross-talk between HP1γ and Utx in controlling histone H3K27 methylation status, thereby define HP1γ as a molecular regulator of germ cell epigenetic reprogramming.
Project description:Affymetrix Hu133 GeneCHIP Microarray data for Control and c-MYC knock-down (KD) human cancer cell lines. Data related to article 'Novel c-MYC target genes mediate differential effects on cell proliferation and migration', from D. CAPPELLEN et al., EMBO Reports Note: Samples GSM136093 and GSM136094 (Hela cell line, expt 1) were hybridized and normalized separately from the other 18 Samples. Keywords: siRNA analysis
