Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: Mitotically associated long non-coding RNA, MANCR regulates cell cycle in triple negative breast cancer cells

OTHER RELATED OMICS DATASETS IN: GSE102155

PROVIDER: PRJNA396880 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5889470.fastq.gz	Fastqsanger.gz
	SRR5889471.fastq.gz	Fastqsanger.gz
	SRR5889466.fastq.gz	Fastqsanger.gz
	SRR5889467.fastq.gz	Fastqsanger.gz
	SRR5889468.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Mitotically associated long non-coding RNA, MANCR regulates cell cycle in triple negative breast cancer cells

Project description:Triple negative breast cancer (TNBC) is an aggressive breast cancer subtype that is difficult to treat as it is unresponsive to hormone-therapy; therefore, it is imperative to identify novel, targetable regulators of progression in TNBC. Long non-coding RNAs (lncRNAs) are important regulators in breast cancer and have great potential as therapeutic targets; however, little is known about how the majority of lncRNAs function within TNBC cells. In this study, we identify a novel lncRNA, MANCR (LINC00704), which is upregulated in TNBC cells and breast cancer patient samples. Depletion of MANCR in TNBC cells results in a significant decrease in cell proliferation and viability with a concomitant increase in DNA damage. Transcriptome-wide sequencing following MANCR knockdown reveals significant differences in the expression of >2000 genes, and gene set enrichment analysis identifies changes in multiple categories related to cell cycle regulation. Furthermore, MANCR expression is highest in mitotic cells by both RT-qPCR and RNA in situ hybridization. Consistent with a possible role in cell cycle regulation, MANCR-depleted cells have a lower mitotic index and a higher incidence of defective cytokinesis. Taken together, our data reveal a role for the novel lncRNA, MANCR (mitotically-associated long non-coding RNA), in cell cycle regulation of aggressive breast cancer, and identify it as a potential therapeutic target.

2018-01-31 | GSE102155 | GEO

Homo sapiens

Project description:Identifying long non-coding RNAs in triple-negative breast cancer

| PRJNA271881 | ENA

E-GEOD-27447

Project description:FZD7 Plays a Critical Role in Triple Negative Breast Cancer Proliferation

2025-01-24 | E-GEOD-27447 | ExpressionAtlas

Long non-coding RNA landscape of patients biopsies from advanced Triple Negative Breast Cancer

Project description:Long non-coding RNA landscape of patients biopsies from advanced Triple Negative Breast Cancer

| PRJNA734951 | ENA

MANCR

Project description:Homo sapiens MANCR, mitotically associated long non coding RNA [Source:HGNC Symbol;Acc:HGNC:44678], is differentially expressed in 24 experiment(s);

| ENSG00000231298 | ExpressionAtlas

MANCR

Project description:Homo sapiens MANCR, mitotically associated long non coding RNA [Source:HGNC Symbol;Acc:HGNC:44678], is expressed in 19 baseline experiment(s);

| ENSG00000231298 | ExpressionAtlas

ADAR1 regulates growth & invasion in triple-negative breast cancer

Project description:ADAR1 catalyzes Adenosine-to-Inosine (A-to-I) editing of double-stranded RNA and regulates global expression output through its interactions with RNA and other proteins. ADARs play important roles in development and disease, and previous work has shown that ADAR1 is oncogenic in a growing list of cancer types. Here we show that ADAR1 is important for growth and invasion in triple negative breast cancer cells, as ADAR1 loss yields reduced growth, migration & invasion, and mammosphere formation. Global RNA-seq analyses demonstrate that ADAR1 regulates both coding and non-coding targets via expression level and/or A-to-I editing. We demonstrated that a recoding edit in FLNB (chr3:58156064) inhibits the tumor suppressive activities of the protein to promote growth & invasion. We show that several tumor suppressor microRNAs are also downregulated by ADAR1 to promote cell cycle progression and invasion. This work describes several novel mechanisms of ADAR1-mediated oncogenesis in triple negative breast cancer, providing support to strategies for targeting ADAR1 in this aggressive cancer type with few treatment options.

2022-03-14 | GSE177056 | GEO

E-GEOD-38959

Project description:Gene expression profiling of triple negative breast cancer, normal ductal cells, and normal tissues

2025-01-24 | E-GEOD-38959 | ExpressionAtlas

Stress-induced lncRNA LAS3 fosters fitness of cancer cells by regulating SART3-mediated spliceosome recycling

Project description:Long non-coding RNAs (lncRNAs) represent a novel class of anti-cancer therapeutic targets. Hypoxia-induced lncRNAs are associated with the aggressive tumor phenotypes and might serve as putative drug targets. Here, we unraveled lncRNAs whose expression is upregulated in hypoxic breast tumors. One of the hypoxia-induced lncRNA, LAS3 (LncRNA Associated to SART3), is commonly upregulated not only in all breast cancer subtypes, but also in several types of epithelial cancers. LAS3 expression is driven by the stress-induced JNK/c-JUN pathway, which is frequently activated in human cancer. By pull down of LAS3 coupled to mass spectrometry-based proteomics, we identified SART3, a component of the splicing machinery, as a LAS3-interacting partner. In a second proteomics experiment, pull down of SART3-containing complexes from MCF10A cells treated with either scramble, or LAS3-specific GapmeRs showed that LAS3 regulates splicing efficiency by triggering SART3 dissociation from the U4/U6 snRNP during the recycling phase of the spliceosome cycle. Finally, differential shotgun analysis of MDA-MB-231/tet-shLAS3 cells allowed us to quantify expression of 2,940 proteins. Here, genes with significant intron retention showed decreased protein expression levels, indicating that widespread LAS3-mediated intron retention disrupts open reading frame integrity leading to stochastic decrease of protein expression and decreased fitness of cancer cells. Together, our data show that LAS3 is essential for growth of LAS3-positive triple negative breast tumors and indicate that LAS3 inhibition might be a suitable therapeutic approach for breast cancer treatment.

2020-05-26 | PXD013334 | Pride

E-MTAB-5243

Project description:Ampliseq transcriptomic array of REF seq. genes in ZEB1 knock out triple negative breast cancer cells

2025-01-23 | E-MTAB-5243 | ExpressionAtlas