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SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth

ABSTRACT: SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth

PROVIDER: PRJNA597771 | ENA |

REPOSITORIES: ENA

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SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth

Project description:Transcriptional profiling of histone methyltransferase SUV39H1-selective small molecule inhibitor F5446-induced genes in human colon carcinoma cells. Tumor cells were treated with F5446 for 48h and used for RNA isolation. The treated cells were compared to untreated control cells. The objective is to identify genes that are regulated by H3K9me3 in the metastatic human colon carcinoma cells.

2019-12-27 | GSE142625 | GEO

SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth.

Project description: Not available

| S-EPMC7138631 | biostudies-literature

Expression data from Adriamycin-treated Emu-myc; Suv39h1-/- B-cell lymphoma

Project description:Oncogene-induced senescence (OIS), a terminal cell cycle block countering (pre)neoplastic lesions, is characterised on the molecular level by trimethylated histone H3 lysine 9 (h3K9me3), a transcriptionally repressive chromatin mark linked to silencing of S-phase-promoting genes. Whether H3K9-governed chromatin remodelling influences anticancer treatment-induced senescence (TIS) and whether functional control of this mark impacts on treatment outcome is not known. We used global gene expression profiling by microarrays to gain insight into the molecular responses of Emu-myc; Suv39h1-/- B-cell lymphoma cells to senescence-inducing anticancer agent Adriamycin (ADR). Primary lymphoma cells isolated from lymph nodes of Emu-Myc; Suv39h1-/- mice were used. In this model, the c-Myc oncogene is constitutively expressed in the cells of the B-cell lineage, leading to spontaneous development of aggressive B-cell lymphomas. Adriamycin (ADR), a cytostatic drug used as a standard part of several lymphoma treatment regimens, is known to massively induce TIS in Suv39h1-proficient lymphomas, protected from apoptosis by Bcl-2 over expression (Myc;Bcl2). In order to discern the impact of Suv39h1 to TIS induction under these conditions, we analysed here transcriptional profiles of matched pairs of Emu-myc;Suv39h1-/-;Bcl2 lymphomas, untreated or treated for 5 days with ADR.

2013-07-04 | E-GEOD-44355 | biostudies-arrayexpress

Colon cancer cells after escape of late apoptosis

Project description:Colon cancer cells after escape of late apoptosis

| PRJNA720553 | ENA

Colon cancer cells after escape of late apoptosis [exp_1]

Project description:In order to explore the potential role of escape of late apoptosis in metastasis, we induced apoptosis and subsequently inhibited the death process in a primary culture of colon cancer cells. Here we wanted to explore the transcriptome of such "undead" cells 7 days after apoptosis induction.

2022-03-08 | GSE171543 | GEO

Effects of SUV39H1 depletion on gene expression in HeLa cells

Project description:HeLa cells were transiently transfected with siRNA against SUV39H1, a histone H3K9 methyltransferase. Several genes were significantly up- or down-regulated. HeLa cells were transiently transfected with siRNA against SUV39H1 or negative control siRNA. Then total RNA was extracted.

2015-08-01 | E-GEOD-59243 | biostudies-arrayexpress

Expression data from senescence-inducible Suv39h1-ERT2 primary mouse Emu-myc B-cell lymphoma

Project description:Treatment-induced senescence (TIS) is a DNA damage-triggered stress-response program, resulting in terminal arrest of affected cells. TIS plays an important role in cancer therapy, as many tumor cells would undergo TIS instead of apoptosis when exposed to standard chemotherapy regimens. The contribution of TIS to overall disease outcome is, however, unclear. To address this, we use lymphoma cells with conditional expression of the senescence-essential factor Suv39h1 (regulatable by 4-hydroxi-tamoxifen). Only cells with active Suv39h1 would undergo TIS in response to chemotherapy. Suv39h1 inactivation during the chemo-treatment would prevent TIS induction, while inactivation in fully senescent cells would allow outgrowth from the TIS cell cycle arrest. Such post-senescent cells (PS) show very different biological behavior than the cells growing in senescence-incompetent setting - never senescent (NS). The molecular characteristics of each of these treatment conditions are analyzed here by assessing global transcriptome data. We used global gene expression profiling by microarrays to gain insight in the molecular programme underlying the chemotherapy response in primary Emu-myc transgenic B-cell lymphomas.

2020-12-31 | GSE133860 | GEO

Colon cancer cells after escape of late apoptosis [exp_1]

Project description:Colon cancer cells after escape of late apoptosis [exp_1]

| PRJNA720012 | ENA

Colon cancer cells after escape of late apoptosis [exp_2]

Project description:Colon cancer cells after escape of late apoptosis [exp_2]

| PRJNA720091 | ENA

Sturgeon chondroitin sulfates inhibit the proliferation of colorectal cancer cells by inducing cell cycle arrest and apoptosis

Project description:Cell proliferation assay and flow cytometric analysis were used to examine the effects of SCS treatment on viability and apoptosis of colon cancer cell HT-29 cells and normal colonic epithelial cell NCM460 cells. Transcriptomic and proteomic studies were used to identify the main targets of SCS. SCS showed little effect on the gene expression profile of NCM460 cells whereas188 genes and 10 proteins were differentially regulated in HT-29 cells after SCS treatment. Enrichment analysis of those genes / proteins showed that majority of them are involved in DNA replication, cell cycle progression, and apoptosis.

2021-09-15 | GSE179862 | GEO

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