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The impact of USP30-AS1 knockdown on gene expression in MDA-MB-231 cell line

ABSTRACT: The impact of USP30-AS1 knockdown on gene expression in MDA-MB-231 cell line

PROVIDER: PRJNA1140862 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30011546_1.fastq.gz	Fastqsanger.gz
	SRR30011546_2.fastq.gz	Fastqsanger.gz
	SRR30011547_1.fastq.gz	Fastqsanger.gz
	SRR30011547_2.fastq.gz	Fastqsanger.gz

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The impact of USP30-AS1 knockdown on gene expression in MDA-MB-231 cell line

Project description:We discovered that USP30-AS1 is significantly upregulated in breast cancer tissues and is closely associated with the cell proliferation signaling pathway. Knockdown of USP30-AS1 notably inhibits cell proliferation in MDA-MB-231 breast cancer cells. USP30-AS1 inhibits the expression of the cell cycle inhibitor p21.

2024-08-31 | GSE273249 | GEO

The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

Project description:Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells.

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The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

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Gene expression data from human breast cancer MDA-MB-231 cells treated with siRNAs targeting long non-coding RNA TMPO-AS1

Project description:To examine the role of long non-coding RNA TMPO-AS1 in breast cancer, MDA-MB-231 cells were treated with siRNAs targeting TMPO-AS1 (siTMPO-AS1) or control siRNA (siControl). 3 samples

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Secretome of control and srGAP1 knockdown MDA-MB-231 cells

Project description:Proteomic of the secretome of control or srGAP knockdown MDA-MB-231 cells

2022-07-11 | PXD026102 | Pride

UGDH knockdown in MDA-MB-231

Project description:UGDH knockdown in MDA-MB-231

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Expression profiles of MDA-MB-231, MDA-231 S1a and S1b

Project description:Identification of genes that are involved in self-seeding by comparing gene expression profiles between parental MDA-MB-231 cells and seeder cells (MDA-231-S1a and S1b) 2 replicates from each sample (parental MDA-MB-231, MDA-MB-231 S1a and MDA-MB-231 S1b) were analyzed

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Sequencing of human breast cancer cell line MDA-MB-231 and its highly pulmonary metastatic subline MDA-MB-231-LM2

Project description:Purpose: Tumor metastasis is the main cause of death from breast cancer patients and cell migration plays a critical role in metastasis. Recent studies have shown long non-coding RNAs (lncRNAs) play an essential role in the initiation and progression of cancer. In the present study, the role of a LncRNA, Rho GTPase Activating Protein 5- Antisense 1 (ARHGAP5-AS1) in breast cancer was investigated. Methods: RNA sequencing was performed to find out dysregulated LncRNAs in MDA-MB-231-LM2 cells. Transwell migration assays and F-actin staining were utilized to estimate cell migration ability. RNA pulldown assays and RNA immunoprecipitation were used to prove the interaction between ARHGAP5-AS1 and SMAD7. Western blot and immunofluorescence imaging were used to examine the protein levels. Dual luciferase reporter assays were performed to evaluate the activation of TGF-β signaling. Results: Compared to MDA-MB-231 cells, the expression of LncRNA ARHGAP5-AS1 (NR_027263) was significantly suppressed in its highly metastatic subtype MDA-MB-231-LM2 cells. Functional study showed ARHGAP5-AS1 could inhibit cell migration via suppression of stress fibers in breast cancer cell lines. Afterwards, SMAD7 was further identified to interact with ARHGAP5-AS1 by its PY motif and thus its ubiquitination and degradation was blocked due to reduced interaction with E3 ligase SMURF1 and SMURF2. Moreover, ARHGAP5-AS1 could inhibit TGF-β signaling pathway due to its inhibitory role on SMAD7. Conclusion: Overall, these findings demonstrate that ARHGAP5-AS1 inhibits breast cancer cell migration and could serve as a novel biomarker for breast cancer metastasis and a potent target for the treatment in the future.

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Effect of FAM83H-AS1 knockdown in MDA-MB-468 cells [cellseq]

Project description:To investigate the role of lncRNA FAM83H-AS1 in breast cancer, we used shRNA to silence FAM83H-AS1 in MDA-MB-468 cells and performed RNA-seq analysis.

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