Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [RNA-Seq]

ABSTRACT: LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [RNA-Seq]

PROVIDER: PRJNA1123007 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29369843_1.fastq.gz	Fastqsanger.gz
	SRR29369843_2.fastq.gz	Fastqsanger.gz
	SRR29369844_1.fastq.gz	Fastqsanger.gz
	SRR29369844_2.fastq.gz	Fastqsanger.gz
	SRR29369845_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [Hi-C]

Project description:LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [Hi-C]

| PRJNA1123006 | ENA

LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [RNA-Seq]

Project description:This study investigates the role of noncoding RNAs in resistance to the anti-androgen drug daro-lutamide in prostate cancer. RNA sequencing identified LOC730101 as a significantly elevated lncRNA in darolutamide-resistant cells. Silencing LOC730101 reduced cell proliferation, indicating its role in drug resistance.

2024-08-15 | GSE269645 | GEO

LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [Hi-C]

2024-08-15 | GSE269644 | GEO

LncRNA LOC730101 Promotes Darolutamide Resistance in Prostate Cancer by Suppressing miR-1-3p.

Project description:Antiandrogen is part of the standard-of-care treatment option for metastatic prostate cancer. However, prostate cancers frequently relapse, and the underlying resistance mechanism remains incompletely understood. This study seeks to investigate whether long non-coding RNAs (lncRNAs) contribute to the resistance against the latest antiandrogen drug, darolutamide. Our RNA sequencing analysis revealed significant overexpression of LOC730101 in darolutamide-resistant cancer cells compared to the parental cells. Elevated LOC730101 levels were also observed in clinical samples of metastatic castration-resistant prostate cancer (CRPC) compared to primary prostate cancer samples. Silencing LOC730101 with siRNA significantly impaired the growth of darolutamide-resistant cells. Additional RNA sequencing analysis identified a set of genes regulated by LOC730101, including key players in the cell cycle regulatory pathway. We further demonstrated that LOC730101 promotes darolutamide resistance by competitively inhibiting microRNA miR-1-3p. Moreover, by Hi-C sequencing, we found that LOC730101 is located in a topologically associating domain (TAD) that undergoes specific gene induction in darolutamide-resistant cells. Collectively, our study demonstrates the crucial role of the lncRNA LOC730101 in darolutamide resistance and its potential as a target for overcoming antiandrogen resistance in CRPC.

| S-EPMC11274508 | biostudies-literature

The key regulation of LncRNA MALAT1/miR-124-3p/PI3K axis during reprogramming of primary mouse hepatocytes into insulin-producing cells

Project description:In this study, a considerable augmentation in the expression of the endogenous long noncoding RNA MALAT1 (lncRNA MALAT1) and PI3K was discerned, in contrast to a significant diminution in miR-124-3p expression, during the progression of in vitro induced differentiation of primary mouse hepatocytes. Bioinformatics scrutiny and the luciferase reporter assay unveiled the binding of miR-124-3p to specific loci in lncRNA MALAT1 and PI3K, suppressing their expression. Elevated expression of lncRNA MALAT1 potently diminished the expression levels of PI3K and attenuated the efficacy of primary mouse hepatocytes differentiation into insulin-producing cells. Furthermore, the in vitro responsiveness of primary mouse hepatocytes-derived β islet-like cells to high glucose stimuli and insulin release by these cells were significantly diminished in the overexpression of lncRNA MALAT1 transfection group, while the outcomes were converse in the si-lncRNA MALAT1 group. The experimental findings suggest that lncRNA MALAT1 effectively sustains PI3K gene expression through competitive binding to miR-124-3p, accomplishing regulation of primary mouse hepatocytes directed β islet-like cell differentiation efficiency.

2025-07-16 | GSE269392 | GEO

GATA2 up-regulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer

Project description:Darolutamide is an anti-androgen drug clinically used for prostate cancer therapy. Despite its efficacy, potential drug resistance poses significant challenges in the clinical setting. To better understand the molecular changes resulting from prolonged exposure to darolutamide, we developed a darolutamide-resistant model using LNCaP prostate cancer cells. Through ChIP-seq analysis, we found that a temporary treatment of cells with darolutamide effectively disrupts AR binding to chromatin. However, in darolutamide-resistant cells, the chromatin binding of AR is largely restored. By an integrative analysis of ChIP-seq and RNA-seq, we further identified GATA2, a pioneer factor for AR, substantially upregulated in darolutamide-resistant cells. GATA2 plays an essential role in promoting the proliferation of darolutamide-resistant cells and directly contributes to drug resistance. The ablation of GATA2 by siRNA abolished AR's recruitment to chromatin, leading to a significant reduction in gene expression regulated by AR in these resistant cells. Conversely, the overexpression of GATA2 in prostate cancer cells promoted cell proliferation and resistance to darolutamide. This study demonstrates the significance of GATA2 in the development of darolutamide resistance and suggests GATA2 as a promising therapeutic target to overcome this resistance.

2024-12-31 | GSE249437 | GEO

PETACC-8 miR-31-3p and miR-31-5p Ancillary Study

Project description:This is a prospective-retrospective study to determine if the expression of the miRNA’s miR-31-3p and miR-31-5p are prognostic of patient outcomes or predictive of the benefit from anti-EGFR therapy in stage III Colon Cancer. The present study will utilize FFPE tumor samples collected from patients enrolled in the PETACC-8 study conducted by the Fédération Francophone de Cancérologie Digestive (FFCD). This phase 3 clinical trial prospectively randomized fully resected stage III colon cancer patients to receive adjuvant treatment with either FOLFOX-4 plus cetuximab or FLOFOX-4 alone.

| 2260465 | ecrin-mdr-crc

GATA2 upregulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer (RNA-Seq)

Project description:Darolutamide is the latest FDA-approved antiandrogen for the treatment of metastatic prostate cancer. Despite its efficacy in prolonging disease-free survival, drug resistance invariably develops. This study aims to understand the molecular mechanisms underlying darolutamide resistance and identify potential therapeutic targets for overcoming the resistance.

2024-12-31 | GSE249436 | GEO

GATA2 upregulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer (ChIP-Seq)

2024-12-31 | GSE249435 | GEO

miR-493-5p, miR-3662, miR-589-3p, human A549 cells, LC-MSMS

Project description:miR-493-5p, miR-3662, and miR-589-3p were estimated as working microRNAs in bleomycin- and methotrexate-induced phenotypic changes in A549 cells via microRNAs-Proteins Analysis of Integrative Relationship (miR-PAIR). To verify the effect of these miRNAs on the their target protein expression levels, comprehensive expression of proteins in A549 cells treated with miR-493-59, miR-3662, and miR-589-3p mimic was examined by SWATH-MS method. As expected by a miR-PAIR mehtod, almost target proteins were succesfully regulated by miR-493-5p and miR-589-3p mimics.

2025-07-25 | PXD053397 | Pride

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