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LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex

ABSTRACT: LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex

PROVIDER: PRJNA894229 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22044008.fastq.gz	Fastqsanger.gz
	SRR22044009.fastq.gz	Fastqsanger.gz
	SRR22044010.fastq.gz	Fastqsanger.gz
	SRR22044011.fastq.gz	Fastqsanger.gz
	SRR22044012.fastq.gz	Fastqsanger.gz

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LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex [circRNA]

Project description:LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex [circRNA]

| PRJNA894231 | ENA

LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex [lncRNA]

Project description:LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex [lncRNA]

| PRJNA894233 | ENA

LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex [miRNA-seq]

Project description:LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex [miRNA-seq]

| PRJNA894232 | ENA

LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-10 | GSE216569 | GEO

LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex [lncRNA]

Project description:To explore the critical non-coding RNAs in the regulation of ferroptosis, we treated panc-1 with cystine depletion.We then performed gene expression profiling analysis using data obtained from RNA-seq of panc-1 cultured normally and panc-1 treated with cystine depletion for 24h in triplicate.

2023-03-10 | GSE216567 | GEO

LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex [circRNA]

2023-03-10 | GSE216566 | GEO

LINC01133 can induce acquired resistance to ferroptosis in pancreatic cancer by enhancing the mRNA stability of FSP1 through forming the LINC01133-FUS-FSP1 complex [miRNA-seq]

2023-03-10 | GSE216568 | GEO

RNA-sequencing of HGC27 cells with and without linc01133 overexpression

Project description:The long intergenic non-coding RNA linc01133 is reported to be oncogenic in various malignancies. However, the role and mechanism of linc01133 in regulating gastric cancer growth is still not clear. In the present study, we found that linc01133 was significantly up-regulated in gastric cancer tissues compared to non-tumorous gastric tissues. Linc01133 over-expression significantly correlated with tumor size and tumor differentiation in gastric cancer patients. The expression of linc01133 was regulated by c-Jun and c-Fos collaboratively. In both in vitro and in vivo studies, linc01133 was shown to promote gastric cancer cell growth. Linc01133 localized in the cytoplasm and functioned as an endogenous competing RNA of miR-145-5p to up-regulate the expression of YES1，which was proved to be the target gene of miR-145-5p. By promoting YES1-dependent YAP1 nuclear translocation, linc01133 up-regulated the expression of the key cell cycle regulators CDK4, CDK6 and cyclin D1 to promote G1-S phase transition. Thus, our study unveiled the function and mechanism of linc01133 regulating cell cycle progression in gastric cancer.

2021-12-21 | GSE191227 | GEO

RNAseq of 4T1 cells expressing exogenous LINC01133

Project description:The PI3K pathway represents the most hyperactivated oncogenic pathway in triple-negative breast cancer (TNBC), a highly aggressive tumor subtype encompassing ~15% of breast cancers with no targeted therapeutics. Despite critical contributions of its signaling arms to disease pathogenesis, PI3K pathway inhibitors have not achieved expected clinical responses in TNBC owing largely to still-incomplete understanding of the compensatory cascades that operate downstream of PI3K. Here, we investigated the contributions of long non-coding RNAs (lncRNAs) to PI3K activities in clinical and experimental TNBC, and discovered a prominent role for LINC01133 as a PI3K-AKT signaling effector. We found that LINC01133 exerted pro-tumorigenic roles in TNBC, and that it governed a previously undescribed mTORC2-dependent pathway that activated AKT in a PI3K-independent manner. Mechanistically, we show that LINC01133 induced the expression of the mTORC2 component PROTOR1/PRR5 by competitively coupling away its negative mRNA regulator, the heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2B1). PROTOR1/PRR5 in turn was sufficient and necessary for LINC01133-triggered functions, casting previously unappreciated roles for this Rictor-binding protein in cellular signaling and growth. Notably, LINC01133 antagonism undermined cellular growth and we show that the LINC01133-PROTOR1/PRR5 pathway tightly associated with TNBC poor patient survival. Altogether, our findings uncovered a lncRNA-driven signaling shunt that acts as a critical determinant of malignancy downstream of the PI3K pathway and as a potential RNA-based theranostic in clinical TNBC management. We performed comparative gene expression profiling analyses using RNA-seq of triplicates of control 4T1 cells (harboring empty plasmid control) and 4T1 cell trioplicates expressing exogenous LINC01133.

2022-10-03 | GSE212004 | GEO

Expression data from Fus/TLS-null KSL hematopoietic stem/progenitor cells

Project description:Fus is the gene for a member of the FET family of RNA-binding proteins often involved in chromosomal translocations to generate oncogenic fusion genes in human cancers. Fus participates in multiple cellular functions, including RNA processing and transport, transcriptional regulation, and genome integrity. We uncovered its critical role in the maintenance of hematopoietic stem cells (HSCs). Fus-/- fetal livers developed normally except for a mild reduction in numbers of colony-forming cells compared to the wild type. The proliferation and differentiation of Fus-/- hematopoietic progenitors were normal in vitro. However, the number of colony-forming cells present in long-term cocultures of Fus-/- hematopoietic progenitors and stromal cells was significantly reduced. Fus-/- HSCs had an impaired long-term repopulating capacity and failed to repopulate in tertiary recipient mice. Fus-/- HSCs were highly susceptible to radiation both in vitro and in vivo and showed retardation of radiation-induced DNA damage repair. These findings define Fus as a novel regulator of HSCs and implicate it in stress-resistance and maintenance of the genomic integrity of HSCs. Therefore, it would be of importance to analyze the gene expression profiles of Fus-knockout hematopoietic stem/progenitor cells to understand its role in HSCs. Purified wild-type and Fus–/– KSL cells from BM of recipient mice repopulated with wild-type and Fus–/– fetal liver cells were subjected to RNA extraction and hybridization on Affymetrix microarrays. Data were obtained from dublicate samples.

2009-11-02 | E-GEOD-18853 | biostudies-arrayexpress

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