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Effects of IFITM1 knockdown in colorectal cancer

ABSTRACT: Interferon-induced transmembrane protein 1 (IFITM1) is one of the three members of the interferon-induced transmembrane family and has recently been identified as a new molecular marker in human colorectal cancer. However, its functional roles in colorectal cancer are still elusive. In this study, we investigate the gene expression profiling of HT-29 cells with IFITM1 knockdown. We revealed that several invasive- and carcinogenesis-related genes were differentially expressed.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20923 | GEO | 2011/03/01

SECONDARY ACCESSION(S): PRJNA124357

REPOSITORIES: GEO

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Effects of IFITM1 knockdown in colorectal cancer

Project description:Interferon-induced transmembrane protein 1 (IFITM1) is one of the three members of the interferon-induced transmembrane family and has recently been identified as a new molecular marker in human colorectal cancer. However, its functional roles in colorectal cancer are still elusive. In this study, we investigate the gene expression profiling of HT-29 cells with IFITM1 knockdown. We revealed that several invasive- and carcinogenesis-related genes were differentially expressed. We transfected siRNAs targeting firefly luciferase and human IFITM1 mRNAs into HT-29 colorectal adenocarcinoma cells. At 72 h post-transfection, total RNA was harvested for microarray hybridization. A siLuc-transfected sample was used as the baseline control.

2011-03-01 | E-GEOD-20923 | biostudies-arrayexpress

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Project description:Analysis of colorectal cancer (CRC) cell line HT-29 treated with Sodium Butyrate. Sodium Butyrate, a HDAC inhibitor present in gut, can differentiate the undifferentiated HT-29 to enterocytes by the induction of brush border enzyme alkaline phosphatase. Results provide the transcriptional profiling underlying the butyrate-induced differentiation of CRC.

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Genome-wide maps of SOX9 binding sites in human colorectal cancer cells

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RNA-seq in HT-29 colorectal cancer cells after F. nucleatum treatment

Project description:To elucidate whether F. nucleatum plays a role in colorectal cancer tumorigenesis, RNA-seq analysis was performed to compare the gene expression profiles of F. nucleatum treated HT-29 cell line or not.

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Interferon-induced transmembrane protein 1 (IFITM1) inhibits Varicella-Zoster Virus Replication

Project description:Interferon-induced transmembrane protein 1 (IFITM1) inhibits Varicella-Zoster Virus Replication

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SRSF1 as a novel interacting partner for IFITM1/3 unravels the emergent role of IFITM1/3 mediating protein expression

Project description:IFITM proteins play a role in cancer cell progression through undefined mechanisms. Recent data demonstrated that interferon induced transmembrane 1 and 3 (IFITM1/3) proteins are required for the interferon gamma (IFNγ) stimulated synthesis of a subset of IFN-stimulated proteins; including human leukocyte antigen B (HLA-B). SBP-tagged IFITM1 protein was used to identify an association of IFITM1 protein with the cytosolic isoform of serine and arginine rich splicing factor 1 (SRSF1). This cytosolic association was confirmed in situ using proximity ligation assays for SRSF1 and IFITM1/3 suggesting a role associated with translation. Accordingly, IFITM1/3 were shown to interact with HLA-B mRNA in response to IFNγ stimulation using RNA-protein proximity ligation assays. In addition, shotgun RNA sequencing in IFITM1/IFITM3 null cells and wt-SiHa cells indicated that reduced HLA-B gene expression does not account for lowered HLA-B protein synthesis in response to IFNγ. Furthermore, ribosome profiling by using sucrose gradient sedimentation identified a reduction in 80S ribosomal fraction an IFITM1/IFITM3 null cells compared to their wild-type counterpart, partially reverted by IFITM1/3 complementation. Taking all together, these data link the binding of IFITM1/3 proteins to HLA-B mRNA and SRSF1 as a mechanism to catalyze the synthesis of target proteins suggesting an RNA chaperonin role for IFITM1/3 proteins.

2022-10-13 | PXD030540 | Pride

The evolution of single cell-derived colorectal cancer cell lines is dominated by the continued selection of tumor specific genomic imbalances, despite random chromosomal instability

Project description:Intratumor heterogeneity is a major challenge in cancer treatment. To decipher patterns of chromosomal heterogeneity, we analyzed six colorectal cancer cell lines by multiplex interphase FISH. The mismatch repair deficient cell lines DLD-1 and HCT116 had the most stable copy numbers, whereas aneuploid cell lines displayed a higher degree of instability. We subsequently assessed the clonal evolution of a single cell in two aneuploid cell lines, SW480 and HT-29, which both have near-triploid karyotypes but different degrees of chromosomal instability. The clonal compositions of the single cell-derived daughter cell lines, as assessed by multiplex FISH, differed for HT-29 and SW480. Daughters of HT-29 were stable, clonal, and had little heterogeneity. Daughters of SW480 were more heterogeneous, with the single cell-derived daughter cell lines separating into two distinct populations with different ploidy (hyper-diploid and near-triploid), morphology, gene expression and tumorigenicity. To better understand the evolutionary trajectory for the two SW480 populations, we constructed phylogenetic trees which showed ongoing instability in the daughter cell lines.. When analyzing the evolutionary development over time, most single cell-derived daughter cell lines maintained their major clonal pattern, with the exception of one daughter of SW480 that showed a switch involving a loss of APC. Our meticulous analysis of the clonal evolution and composition of these colorectal cancer models shows that all chromosomes are subject to segregation errors, however, specific net genomic imbalances are maintained. Karyotype evolution is driven by the necessity to arrive at and maintain a specific plateau of chromosomal copy numbers as the drivers of carcinogenesis.

2018-05-01 | GSE102647 | GEO

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