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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]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE216566 | GEO | 2023/03/10

REPOSITORIES: GEO

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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 [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 [miRNA-seq]

2023-03-10 | GSE216568 | GEO

LINC01133 can induce acquired ferroptosis resistance by enhancing the FSP1 mRNA stability through forming the LINC01133-FUS-FSP1 complex.

Project description:Due to a lack of research on the critical non-coding RNAs in regulating ferroptosis, our study aimed to uncover the crucial ones involved in the process. We found that LINC01133 could make pancreatic cancer cells more resistant to ferroptosis. A higher expression of LINC01133 was associated with a higher IC50 of sorafenib in clinical samples. Furthermore, we discovered that LINC01133 induced this process through enhancing the mRNA stability of FSP1. CEBPB was the transcription factor to increase the expression of LINC01133. A higher CEBPB could also indicate a higher IC50 of sorafenib in patients with cancer. Moreover, we confirmed that LINC01133 could form a triple complex with FUS and FSP1 to increase the mRNA stability of FSP1.

| S-EPMC10676390 | biostudies-literature

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 [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

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

| PRJNA894229 | 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

Identification of circRNA-interacting proteins in pancreatic ductal adenocarcinoma

Project description:Many studies have demonstrated the importance of circRNA in regulating gene expression through functioning as microRNA sponges. However, the roles of circRNA-protein interaction are not fully understood. Importantly, how circRNA-protein interaction contributes the progression of pancreatic ductal adenocarcinoma is largely unexplored. Therefore, RNA Pull down assay for investigating RNA-protein interaction was performed in PANC-1 cells.

2022-02-15 | PXD015048 | Pride

FUS Alters circRNA Metabolism in Human Motor Neurons Carrying the ALS-Linked P525L Mutation.

Project description:Deregulation of RNA metabolism has emerged as one of the key events leading to the degeneration of motor neurons (MNs) in Amyotrophic Lateral Sclerosis (ALS) disease. Indeed, mutations on RNA-binding proteins (RBPs) or on proteins involved in aspects of RNA metabolism account for the majority of familiar forms of ALS. In particular, the impact of the ALS-linked mutations of the RBP FUS on many aspects of RNA-related processes has been vastly investigated. FUS plays a pivotal role in splicing regulation and its mutations severely alter the exon composition of transcripts coding for proteins involved in neurogenesis, axon guidance, and synaptic activity. In this study, by using in vitro-derived human MNs, we investigate the effect of the P525L FUS mutation on non-canonical splicing events that leads to the formation of circular RNAs (circRNAs). We observed altered levels of circRNAs in FUSP525L MNs and a preferential binding of the mutant protein to introns flanking downregulated circRNAs and containing inverted Alu repeats. For a subset of circRNAs, FUSP525L also impacts their nuclear/cytoplasmic partitioning, confirming its involvement in different processes of RNA metabolism. Finally, we assess the potential of cytoplasmic circRNAs to act as miRNA sponges, with possible implications in ALS pathogenesis.

| S-EPMC9968238 | biostudies-literature

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