Gene expression profile of colorectal carcinoma HT29 PARP13 KO cells treated with fractionated ionizing radiation dose (5x2Gy) under 2D or 3D cell culture conditions
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PROVIDER: PRJNA1177864 | ENA |
REPOSITORIES: ENA
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Project description:Radiotherapy is one of the most common treatments for cancer. The effects of IR are dose-dependent and different cell types have different sensitivities to IR. To reduce the damage of IR to the most sensitive cells of normal tissue, radiotherapy is administered as a fractionated dose treatment, delivering radiation in 2 Gy fractions every 24 hours, 5 times a week. However, during the course of therapy, intrinsic and acquired radioresistance of the tumor can lead to treatment failure. Therefore, there is a need for combination therapy including radiotherapy and targeted anticancer treatment. In the present study, we investigated global gene expression changes in colorectal cancer HT29 PARP13 KO cells after X-ray irradiation with a fractionated dose of 5 x 2 Gy. Agilent microarray technology was used to analyze gene expression levels in cells cultured under 2D and 3D culture conditions.
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Project description:Among the key players in the DDR networks are members of the 17 PARP (poly-ADP-ribose polymerase) protein family. Beyond their involvement in various biological processes - such as transcription control, cell death, and inflammation – some PARPs specifically contribute to attracting repair proteins to sites of DNA damage. PARP1 and PARP2, the most well-studied members, act as DNA damage sensors and signal transducers synthesizing poly-ADP-ribose chains that recruits DNA repair factors and can remodel chromatin structure around damaged DNA. In addition to the well-characterized PARPs, other members of this family hold promise for cancer therapeutic applications as they are also involved in the DNA damage response. In the present study, we investigated PARP13-dependent changes in gene expression in colorectal carcinoma HT29 cell lines. Agilent microarray technology was used to analyze gene expression levels in cells cultured under 2D and 3D culture conditions. The results of our study demonstrate the pivotal role of PARP13 in the immune response and the potential for using this target for therapeutic purposes. The profile of differentially expressed genes identified in the present study could be used for further development of diagnostic and therapeutic applications in CRC.
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Project description:Tumor cell response to irradiation also depends on their microenvironment. Therefore ongoing investigation of three-dimensional (3D) cell culture models provide researchers with essential data studying and remodeling radiotherapeutic implications in cancer treatment. 3D culture models were shown to mimic in vivo cell microenvironment more accurately than the standard two-dimensional cell monolayer (2D) cultures. Growing evidence suggests that 2D and 3D cultured cell gene expression pattern discrepancies following irradiation is highly dependent on cell-ECM interactions. It has been shown that laminin-rich-extracellular matrix (lr-ECM) used in 3D cultures not only alters cancer cell phenotype and response to external stimuli but also affects their differentiation, migration and survivability. Thus, a change in these fundamental cell properties demands us to reconsider data previously collected using 2D in vitro models. RNA was harvested from two colorectal cancer cell lines cultivated under 3D cell culture conditions, 4h after treatment of single (2 Gy or 10 Gy) or fractionated (5x2 Gy) ionizing radiation dose.
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Project description:Gene expression profile of colorectal carcinoma HT29 PARP13 KO cells cultivated in 2D or 3D cell culture models
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Project description:Poly(ADP-ribose) Polymerase-13 (PARP13/ZAP/ZC3HAV1) is an antiviral factor, active against specific RNA viruses such as MLV, SINV and HIV. During infection PARP13 binds viral RNA via its 4 CCCH-type zinc finger domains and targets it for degradation by recruiting cellular mRNA decay factors such as the exosome complex and XRN1. Here we show that PARP13 binds to and regulates cellular mRNA under physiological conditions. Knock-down of PARP13 via RNAi results in the misregulation of hundreds of transcripts with an enrichment in signal peptide containing proteins. Among the most upregulated transcripts is TRILR4
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Project description:The RNA-binding protein PARP13 is a primary factor in the innate antiviral response. PARP13 can suppress translation and drive decay of bound viral and host RNA. PARP13 interacts with many proteins encoded by interferon-stimulated genes (ISG) to perform its antiviral activities, such as activation of the pathway mediated by post-translational addition ISG15 or ISGylation. The RNA-binding domains of both PARP13 and its primary cofactor, TRIM25, are required for antiviral activity. Here we perform enhanced crosslinking immunoprecipitation (eCLIP) and RNA-seq to investigate the role of PARP13 expression and RNA binding in transcriptome regulation within human cells. We find that PARP13 regulates the transcriptome in basal and antiviral states and that the antiviral response shifts PARP13 target localization, but not its binding preferences. We demonstrate that PARP13 expression supports the expression of ISGylation-related genes, including TRIM25. Using the common targets PARP13 and TRIM25 share, we assess their spatial relationship along transcripts and show that PARP13 and TRIM25 associate in part via RNA-protein interactions. Evidence from genomic data and molecular biology experiments provide insight into the geometry of PARP13's interface with its cofactor TRIM25 and implicates PARP13 in creating and maintaining a cellular environment poised for an antiviral response.
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Project description:The RNA-binding protein PARP13 is a primary factor in the innate antiviral response. PARP13 can suppress translation and drive decay of bound viral and host RNA. PARP13 interacts with many proteins encoded by interferon-stimulated genes (ISG) to perform its antiviral activities, such as activation of the pathway mediated by post-translational addition ISG15 or ISGylation. The RNA-binding domains of both PARP13 and its primary cofactor, TRIM25, are required for antiviral activity. Here we perform enhanced crosslinking immunoprecipitation (eCLIP) and RNA-seq to investigate the role of PARP13 expression and RNA binding in transcriptome regulation within human cells. We find that PARP13 regulates the transcriptome in basal and antiviral states and that the antiviral response shifts PARP13 target localization, but not its binding preferences. We demonstrate that PARP13 expression supports the expression of ISGylation-related genes, including TRIM25. Using the common targets PARP13 and TRIM25 share, we assess their spatial relationship along transcripts and show that PARP13 and TRIM25 associate in part via RNA-protein interactions. Evidence from genomic data and molecular biology experiments provide insight into the geometry of PARP13's interface with its cofactor TRIM25 and implicates PARP13 in creating and maintaining a cellular environment poised for an antiviral response.
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Project description:Radiotherapy is one of the most common therapies for cancer. Approximately half of all cancer patients will receive radiotherapy at some point during treatment. Consequences of IR treatment are dose dependent and different sensitivity to IR of various types of cells is well established. To reduce the damage of IR to most sensitive cells of normal (noncancerous) tissue radiotherapy is administered as fractionated dose treatment applying radiation in ~2 Gy fractions every 24 hours, 5 times per week. However, during the therapy intrinsic and acquired tumor radioresistance may result in treatment failures. Comprehensive mechanisms of the resistance to irradiation as well as mechanisms of cellular response to fractionated dose IR remain unclear. Therefore, in the present study we evaluated global gene expression changes in murine Lewis lung carcinoma LLC1 cells following X-ray irradiation of single 2 Gy or 10 Gy and 2 Gy x 5 fractionated doses. Total RNA was harvested from mouse Lewis lung carcinoma cells 4h after treatment of single (2 Gy or 10 Gy) or fractionated (5x2 Gy) ionizing radiation dose.
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Project description:Radiotherapy is one of the most common therapies for cancer. Approximately half of all cancer patients will receive radiotherapy at some point during treatment. Consequences of IR treatment are dose dependent and different sensitivity to IR of various types of cells is well established. To reduce the damage of IR to most sensitive cells of normal (noncancerous) tissue radiotherapy is administered as fractionated dose treatment applying radiation in ~2 Gy fractions every 24 hours, 5 times per week. However, during the therapy intrinsic and acquired tumor radioresistance may result in treatment failures. Comprehensive mechanisms of the resistance to irradiation as well as mechanisms of cellular response to fractionated dose IR remain unclear. Different gene expression patterns may be partially influenced by short ~22 nt non-coding RNA molecules called microRNAs (miRNAs) via translational regulation or RNA degradation mechanisms. Therefore, in the present study we evaluated global miRNA changes in murine Lewis lung carcinoma LLC1 cells following X-ray irradiation of single 2 Gy or 10 Gy and 2 Gy x 5 fractionated doses. Total RNA enriched in small noncoding RNAs was isolated from mouse Lewis lung carcinoma cells 4h after treatment of single (2 Gy or 10 Gy) or fractionated (5x2 Gy) ionizing radiation dose.
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