LYAR promotes colorectal cancer progression by up-regulating FSCN1 expression and fatty acid metabolism
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ABSTRACT:
PROVIDER: PRJNA747285 | ENA |
REPOSITORIES: ENA
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Project description: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.
2021-07-17 | GSE180263 | GEO
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
Project description:LYAR promotes colorectal cancer progression by up-regulating FSCN1 expression and is closely related to fatty acid metabolism
| PRJNA749594 | ENA
Project description: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, is expressed at a higher level in CRC tissue than in adjacent normal tissue and that LYAR expression is closely associated with distant CRC metastasis. LYAR not only significantly promotes the migration and invasion of CRC cells in vitro, but knockdown (KD) of LYAR in CRC cells also inhibits xenograft tumor metastasis in vivo. Microarray analysis of LYAR KD cells combined with a chromatin immunoprecipitation (ChIP) assay, gene reporter assay, and rescue experiment indicated that FSCN1 (encoding fascin actin-bundling protein 1 (Fascin-1)) serves as a novel key regulator of LYAR-promoted migration and invasion of CRC cells. Knockdown of FSCN1 significantly inhibits subcutaneous tumorigenesis of CRC cells and leads to the downregulation 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 upregulating FSCN1 expression and affecting fatty acid metabolism in CRC.
| S-EPMC8769847 | biostudies-literature
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
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
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
Project description:Wnt signaling is critical for normal skeletal development as well as whole-body metabolic function. In this study, we described a previously unrecognized function for Wnt-Lrp5 signaling in the osteoblast that allows bone to acquire the resources necessary to fuel bone formation. Mice lacking the Lrp5 co-receptor specifically in osteoblasts and osteocytes exhibit the expected reductions in postnatal bone mass and also develop peripheral adiposity with corresponding reductions in energy expenditure. Conversely, mice expressing a high-bone mass mutant Lrp5 allele are leaner with reduced plasma triglyceride and free fatty acid levels. In this context, Wnt-initiated signals downstream of Lrp5, but not Lrp6, regulate the expression of key enzymes required for fatty acid β-oxidation. These results suggest that Wnt-Lrp5 signaling regulates basic cellular activities beyond those associated with fate-specification and differentiation in bone and that the skeleton influences global energy homeostasis via mechanisms independent of osteocalcin and glucose metabolism Total RNA isolated from cultures of Lrp5-deficient osteoblasts differentiated for 7 days in vitro compared to control osteoblasts
2014-03-14 | E-GEOD-55900 | biostudies-arrayexpress
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
Project description:To explore the downstream molecules of FSCN1, shRNA targeting FSCN1 was designed and transfected into the ESCC cell line, ECA-109. Whole-genome expression profiling was performed to screen for related molecules. 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, and the associated RNA was analyzed by RNA-seq.
2022-03-05 | GSE197624 | GEO