Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Next Generation Sequencing Facilitates Quantitative Analysis of chromatin conformational interaction between MYC and PVT1 in MDA-MB-231, MCF7, HCT116 cancer cell line

ABSTRACT: MYC-PVT1 interaction is cell line specific

ORGANISM(S): Homo sapiens

PROVIDER: GSE97588 | GEO | 2018/05/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Next Generation Sequencing Facilitates Quantitative Analysis of chromatin conformational interaction between MYC and PVT1 in MCF7

Project description:MYC-PVT1 interaction is cell line specific

2018-05-31 | GSE106153 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of PVT1 overexpressed MDA-MB-231 cells.

Project description:PVT1 can regulates glycolysis related genes expression.

2024-05-01 | GSE175736 | GEO

Next Generation Sequencing for Chromatin accessbility by ATAC-seq for MDA-MB-231, MCF7 or HCT116 cell line

Project description:CRISPRi on PVT1 did not induce drastic changes on chromatin accessbility in MDA-MB-231 cell line. CCAT1 enhancer is accessble specifically in HCT116, not in MCF7 or MDA-MB-231.

2018-05-31 | GSE97583 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis for Chromatin Immunoprecipitation of Wild Type and PVT1 Knockdown by CRISPRi in MDA-MB-231 human breast cancer cell line

Project description:CRISPRi targeting PVT1 specifically increased H3K9me3 at PVT1

2018-05-31 | GSE97584 | GEO

Simultaneous defeat of MCF7 and MDA-MB-231 resistances by a hypericin PDT-tamoxifen hybrid therapy.

Project description:Currently the greatest challenge in oncology is the lack of homogeneity of the lesions where different cell components respond differently to treatment. There is growing consensus that monotherapies are insufficient to eradicate the disease and there is an unmet need for more potent combinatorial treatments. We have previously shown that hypericin photodynamic therapy (HYP-PDT) triggers electron transport chain (ETC) inhibition in cell mitochondria. We have also shown that tamoxifen (TAM) enhances cytotoxicity in cells with high respiration, when combined with ETC inhibitors. Herein we introduce a synergistic treatment based on TAM chemotherapy and HYP-PDT. We tested this novel combinatorial treatment (HYPERTAM) in two metabolically different breast cancer cell lines, the triple-negative MDA-MB-231 and the estrogen-receptor-positive MCF7, the former being quite sensitive to HYP-PDT while the latter very responsive to TAM treatment. In addition, we investigated the mode of death, effect of lipid peroxidation, and the effect on cell metabolism. The results were quite astounding. HYPERTAM exhibited over 90% cytotoxicity in both cell lines. This cytotoxicity was in the form of both necrosis and autophagy, while high levels of lipid peroxidation were observed in both cell lines. We, consequently, translated our research to an in vivo pilot study encompassing the MDA-MB-231 and MCF7 tumor models in NOD SCID-? immunocompromised mice. Both treatment cohorts responded very positively to HYPERTRAM, which significantly prolonged mice survival. HYPERTAM is a potent, synergistic modality, which may lay the foundations for a novel, composite anticancer treatment, effective in diverse tumor types.

| S-EPMC6458138 | biostudies-literature

Telomerase Inhibitor TMPyP4 Alters Adhesion and Migration of Breast-Cancer Cells MCF7 and MDA-MB-231.

Project description:Human telomeres were one of the first discovered and characterized sequences forming quadruplex structures. Association of these structures with oncogenic and tumor suppressor proteins suggests their important role in cancer development and therapy efficacy. Since cationic porphyrin TMPyP4 is known as G-quadruplex stabilizer and telomerase inhibitor, the aim of the study was to analyze the anticancer properties of this compound in two different human breast-cancer MCF7 and MDA-MB-231 cell lines. The cytotoxicity of TMPyP4 alone or in combination with doxorubicin was measured by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromid) and clonogenic assays, and the cell-cycle alterations were analyzed by flow cytometry. Telomerase expression and activity were evaluated using qPCR and telomeric repeat amplification protocol (TRAP) assays, respectively. The contribution of G-quadruplex inhibitor to protein pathways engaged in cell survival, DNA repair, adhesion, and migration was performed using immunodetection. Scratch assay and functional assessment of migration and cell adhesion were also performed. Consequently, it was revealed that in the short term, TMPyP4 neither revealed cytotoxic effect nor sensitized MCF7 and MDA-MB-231 to doxorubicin, but altered breast-cancer cell adhesion and migration. It suggests that TMPyP4 might substantially contribute to a significant decrease in cancer cell dissemination and, consequently, cancer cell survival reduction. Importantly, this effect might not be associated with telomeres or telomerase.

| S-EPMC6600420 | biostudies-literature

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and PVT1 Knockdown by CRISPRi in MDA-MB-231 human breast cancer cell line

Project description:Induced MYC expression by CRISPRi targeting PVT1 was validated by RNA-seq

2018-05-31 | GSE97587 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis for H3K27ac mediated chromatin conformation capture of Wild Type and PVT1 Knockdown by CRISPRi in MDA-MB-231 human breast cancer cell line

Project description:CRISPRi targeting PVT1 specifically decrease PVT1-MYC interaction

2018-05-31 | GSE97585 | GEO

Adipose MSCs Suppress MCF7 and MDA-MB-231 Breast Cancer Metastasis and EMT Pathways Leading to Dormancy via Exosomal-miRNAs Following Co-Culture Interaction.

Project description:Globally, breast cancer is the most frequently diagnosed cancer in women, and it remains a substantial clinical challenge due to cancer relapse. The presence of a subpopulation of dormant breast cancer cells that survived chemotherapy and metastasized to distant organs may contribute to relapse. Tumor microenvironment (TME) plays a significant role as a niche in inducing cancer cells into dormancy as well as involves in the reversible epithelial-to-mesenchymal transition (EMT) into aggressive phenotype responsible for cancer-related mortality in patients. Mesenchymal stem cells (MSCs) are known to migrate to TME and interact with cancer cells via secretion of exosome- containing biomolecules, microRNA. Understanding of interaction between MSCs and cancer cells via exosomal miRNAs is important in determining the therapeutic role of MSC in treating breast cancer cells and relapse. In this study, exosomes were harvested from a medium of indirect co-culture of MCF7-luminal and MDA-MB-231-basal breast cancer cells (BCCs) subtypes with adipose MSCs. The interaction resulted in different exosomal miRNAs profiles that modulate essential signaling pathways and cell cycle arrest into dormancy via inhibition of metastasis and epithelial-to-mesenchymal transition (EMT). Overall, breast cancer cells displayed a change towards a more dormant-epithelial phenotype associated with lower rates of metastasis and higher chemoresistance. The study highlights the crucial roles of adipose MSCs in inducing dormancy and identifying miRNAs-dormancy related markers that could be used to identify the metastatic pattern, predict relapses in cancer patients and to be potential candidate targets for new targeted therapy.

| S-EPMC7824212 | biostudies-literature

Next Generation Sequencing Facilitates Quantitative Analysis of chromatin conformational interaction between MYC and PVT1 in MCF7

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of chromatin conformational interaction between MYC and PVT1 in MCF7

| PRJNA415772 | ENA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data