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LYAR promotes colorectal cancer progression by up-regulating FSCN1 expression and fatty acid metabolism

ABSTRACT: Colorectal cancer (CRC) is a highly malignant tumor associated with poor prognosis, yet the molecular mechanisms are not fully understood. In this study, we showed that LYAR, a nucleolar protein, expresses at a higher level in CRC than adjacent normal tissue and LYAR expression is closely associated with distant CRC metastasis. LYAR not only significantly promotes the migration and invasion of CRC cells in vitro, also the knockdown (KD) of LYAR in CRC cells inhibits xenograft tumor metastasis in vivo. Microarray analysis of LYAR KD cells combined with ChIP assay, gene reporter assay and rescue experiment indicate that FSCN1 (encoding fascin actin-bundling protein 1, Fascin-1) serves as a new key regulator of the LYAR-promoted migration and invasion of CRC cells. Knockdown of FSCN1 significantly inhibits subcutaneous tumorigenesis of CRC cells, and leads to the down-regulation of FASN and SCD, genes encoding key enzymes in fatty acid synthesis. In summary, this study reveals a novel mechanism by which LYAR promotes tumor cell migration and invasion by up-regulating FSCN1 expression and affecting fatty acid metabolism in CRC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE180263 | GEO | 2021/07/17

REPOSITORIES: GEO

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LYAR promotes colorectal cancer progression by up-regulating FSCN1 expression and is closely related to fatty acid metabolism

Project description:Colorectal cancer (CRC) is a highly malignant tumor associated with a poor prognosis, yet the molecular mechanisms are not fully understood. In this study, we showed that LYAR expresses at a higher level in CRC than normal tissue and LYAR expression is closely associated with distant CRC metastasis. LYAR significantly promotes the migration and invasion of CRC cells in vitro, and reduction of LYAR expression in CRC cells inhibites xenograft tumor metastasis in vivo. Microarray analysis of LYAR knockdown (KD) cells combined with ChIP assay, gene reporter assay and rescue experiment indicate that FSCN1 (fascin actin-bundling protein 1, Fascin-1) serves as a new and key regulator of the LYAR-promoted migration and invasion of CRC cells. In addition, knockdown of FSCN1 significantly inhibites subcutaneous tumorigenesis of CRC cells. Moreover, we found that FSCN1 affects some key enzymes in lipid fatty acid metabolism such as FASN and SCD. In summary, this study reveals a novel mechanism by which LYAR promotes tumor cell migration and invasion by up-regulating FSCN1 expression and further promoting fatty acid synthesis in CRC.

2021-07-26 | GSE180805 | GEO

Proteomic Analysis of FSCN1-Interacting Proteins in LSCC cells

Project description:Fascin actin-bundling protein 1 (FSCN1) is an evolutionarily conserved actin-bundling protein that plays a critical role in cell migration, motility, adhesion and cellular interactions. Although multiple clinical studies have implicated the expression of FSCN1 in laryngeal squamous cell carcinoma (LSCC) progression, the precise mechanism of FSCN1 in the process has not been clearly elucidated. To define FSCN1 function, we characterized FSCN1-interacting proteins in LSCC cells by immunoprecipitation followed by LC-MS/MS. After data filtering, 119 proteins with expression in both the Hep-2 and TU-177 cell samples were identified as FSCN1-interacting partners. With in-depth bioinformatics analysis, we linked FSCN1 to critical cellular processes including cell adhesion, glycolysis/gluconeogenesis, regulation of protein ubiquitination, ribosomal RNA processing and small molecule metabolism. We discuss the interactions between FSCN1 and some of the newly validated partners. The identification of these potential partners of FSCN1 expands our knowledge of the FSCN1 interactome and provides a valuable resource for understanding the functions of this protein in LSCC progression.

2019-09-09 | PXD013072 | Pride

Effect of FSCN1 gene inactivation in the H295R cell line

Project description:The actin-bundling protein fascin (FSCN1) is overexpressed in aggressive adrenocortical carcinoma (ACC) and represents a reliable prognostic indicator. We investigated the effects of FSCN1 inactivation by CRISPR/Cas9 in ACC H295R cells on global gene expression profiles in those cells. We performed gene expression profiling analysis using data obtained from RNA-seq of 2 different H295R control clones and 2 different FSCN1 KO clones (2 biological replicates for each clone).

2022-10-25 | GSE216008 | GEO

Screening of differentially expressed genes in LSCC cells knocking down FSCN1

Project description:Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumor with a poor prognosis. Fascin actin-bundling protein 1 (FSCN1) has been reported to play a crucial role in LSCC development and progression, but the underlying molecular mechanisms remain unknown. Here, a whole transcriptome microarray analysis was performed to screen for differentially expressed genes in FSCN1 knockdown cells. We identified 1063 differentially expressed mRNA transcripts. Functional annotation revealed that these differentially expressed genes (DEGs) were involved in multiple biological functions such as transcriptional regulation, response to radiation, focal adhesion, ECM-receptor interaction, steroid biosynthesis, and others. Through co-expression and protein-protein interaction analysis, we linked FSCN1 to novel functions, including defense response to virus and steroid biosynthesis.

2024-02-17 | GSE255143 | GEO

Effects of FSCN1 inactivation on protein expression in human adrenocortical cancer cells

Project description:Adrenocortical carcinoma (ACC) is a rare endocrine malignancy with a high risk of relapse and metastatisation. The actin-bundling protein fascin (FSCN1) is overexpressed in aggressive ACC and represents a reliable prognostic indicator. FSCN1 has been shown to synergize with the Rho/Rac GEF VAV2 in enhancing the invasion properties of ACC cancer cells. Based on those results, we investigated the effects of FSCN1 inactivation by CRISPR/Cas9 or pharmacological blockade on the invasive properties of ACC cells, both in vitro and in an in vivo metastatic ACC zebrafish model. Moreover, to assess the impact of FSCN1 inactivation on global gene and protein expression in H295R cells, we performed RNA-seq and proteomic profiling of control and FSCN1 knock-out (KO) clones.

2022-11-18 | MSV000090738 | MassIVE

Genome-wide analysis of gene expression regulated by FSCN1 in cervical cancer HeLa cells

Project description:FSCN1 has been reported to be dysregulated in cervical cancers. However, the genome-wide regulated targets of FSCN1 is still unclear in cervical cancers. Here, the gene expression profile of HeLa cells transfected with FSCN1 shRNA (shFSCN1) were compared with cells transfected with empty vector (shCtrl). The results showed that shFSCN1 extensively affects the transcriptional level of 5, 043 genes in HeLa cells. There were more up-regulated genes (3, 870) than down-regulated ones (1, 173) after FSCN1 was knocked down in HeLa cells. GO analysis showed that the up-regulated genes were associated with transcription regulation and DNA binding. The down-regulated genes were enriched in some cancer associated pathway including angiogenesis and cell adhesion. In particular, FSCN1 positilvely regulated ANGPTL4 in HeLa cells. Compared to normal tissue, both FSCN1 and ANGPTL4 showed a higher expression in cervical tumor tissue. Moreover, ANGPTL4 was also positilvely correlated with expression of FSCN1 in cervical tumor tissue of TCGA. In conclusion, our study provide important cues for further study on the regulatory mechanism of FSCN1 in cervical cancer.

2022-01-20 | GSE149450 | GEO

Fascin actin-bundling protein 1 regulates non-small cell lung cancer progression by influencing transcription and splicing of tumorigenesis-related genes [IRIP-seq]

Project description:Background. High mortality rates are prevalent among patients with non-small cell lung cancer (NSCLC), and effective therapeutic targets are key prognostic factors. Fascin actin-bundling protein 1 (FSCN1) promotes NSCLC; however, its role as an RNA-binding protein in NSCLC remains unexplored. Therefore, we aimed to explore FSCN1 expression and function in A549 cells. Method. We screened for alternative-splicing events and differentially expressed genes (DEGs) after FSCN1 silence via RNA-sequencing (RNA-seq). FSCN1 immunoprecipitation followed by RNA-seq were used to identify target genes whose mRNA expression and pre-mRNA alternative-splicing levels might be influenced by FSCN1. Results. Silencing FSCN1 in A549 cells affected malignant phenotypes; it inhibited proliferation, migration, and invasion, and promoted apoptosis. RNA-seq analysis revealed 2851 DEGs and 3057 alternatively spliced genes. Gene ontology-based functional enrichment analysis showed that downregulated DEGs and alternatively splicing genes were enriched for the cell-cycle. FSCN1 promoted the alternative splicing of cell-cycle-related mRNAs involved in tumorigenesis (i.e., BCCIP, DLGAP5, PRC1, RECQL5, WTAP, and SGO1). Combined analysis of FSCN1 RNA-binding targets and RNA-seq data suggested that FSCN1 might affect ACTG1, KRT7, and PDE3A expression by affecting the pre-mRNA alternative-splicing levels of NME4, NCOR2, and EEF1D FSCN1 to long non-coding RNA transcripts (RNASNHG20, NEAT1, NSD2, and FTH1), which were highly abundant. Overall, extensive transcriptome analysis of gene alternative splicing and expression levels was performed in cells transfected with FSCN1 short-interfering RNA. Our data provide global insights into the regulatory mechanisms mediated by FSCN1 and its target genes in lung cancer.

2023-07-01 | GSE234858 | GEO

Fascin actin-bundling protein 1 regulates non-small cell lung cancer progression by influencing transcription and splicing of tumorigenesis-related genes [RNA-seq]

2023-07-01 | GSE234859 | GEO

Tumor microenvironment and transcriptional analysis of CD45+ leukocytes isolated from syngeneic MC38 tumors from mice fed ketogenic diet or control diet

Project description:Tumor microenvironment (TME) has a dynamic composition that affects targeted therapies for colorectal cancer (CRC). Cancer associated fibroblasts (CAFs) direct and induce infiltration of immunosuppressive cells through secreted cytokines such as CXCL12. Here, we show that decreased ketogenesis is a signature of CRCs and that an increase in ketogenesis, using a ketogenic diet (KD), decreases CXCL12 in CAFs, tumors, serum, livers, and lungs. Increase in ketogenesis results in the decreased expression of KLF5, which binds to the CXCL12 promoter and induces CXCL12 expression. KD decreases intratumoral accumulation of M2 macrophages and myeloid-derived suppressor cells (MDSCs), increases infiltration of NK and cytotoxic T cells and enhances the anticancer effects of PD-1 blockade in murine-derived CRCs. Moreover, an increase in ketogenesis inhibits CRC migration, invasion, and metastasis in vitro and in vivo. Importantly, our studies demonstrate that downregulation of de novo ketogenesis in the TME is a critical step in CRC progression.

2022-04-27 | GSE180110 | GEO

the RNA binding property of FSCN1

Project description:To investigate the RNA binding property of FSCN1 in ESCC, RNA immunoprecipitation (RIP) was performed using an FSCN1 monoclonal antibody in ECA-109 cell lysate

2022-03-05 | GSE197621 | GEO

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