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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

FSP1 oxidizes NADPH to suppress ferroptosis.

Project description: Not available

| S-EPMC10709417 | biostudies-literature

Phase separation of FSP1 promotes ferroptosis.

Project description:Ferroptosis is evolving as a highly promising approach to combat difficult-to-treat tumour entities including therapy-refractory and dedifferentiating cancers1-3. Recently, ferroptosis suppressor protein-1 (FSP1), along with extramitochondrial ubiquinone or exogenous vitamin K and NAD(P)H/H+ as an electron donor, has been identified as the second ferroptosis-suppressing system, which efficiently prevents lipid peroxidation independently of the cyst(e)ine-glutathione (GSH)-glutathione peroxidase 4 (GPX4) axis4-6. To develop FSP1 inhibitors as next-generation therapeutic ferroptosis inducers, here we performed a small molecule library screen and identified the compound class of 3-phenylquinazolinones (represented by icFSP1) as potent FSP1 inhibitors. We show that icFSP1, unlike iFSP1, the first described on-target FSP1 inhibitor5, does not competitively inhibit FSP1 enzyme activity, but instead triggers subcellular relocalization of FSP1 from the membrane and FSP1 condensation before ferroptosis induction, in synergism with GPX4 inhibition. icFSP1-induced FSP1 condensates show droplet-like properties consistent with phase separation, an emerging and widespread mechanism to modulate biological activity7. N-terminal myristoylation, distinct amino acid residues and intrinsically disordered, low-complexity regions in FSP1 were identified to be essential for FSP1-dependent phase separation in cells and in vitro. We further demonstrate that icFSP1 impairs tumour growth and induces FSP1 condensates in tumours in vivo. Hence, our results suggest that icFSP1 exhibits a unique mechanism of action and synergizes with ferroptosis-inducing agents to potentiate the ferroptotic cell death response, thus providing a rationale for targeting FSP1-dependent phase separation as an efficient anti-cancer therapy.

| S-EPMC10338336 | biostudies-literature

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