Experimental study of plasma 3’tiRNA-CysGCA as a novel molecular marker for damp-heat induced colorectal cancer
Ontology highlight
ABSTRACT:
DISEASE(S): Colorectal Cance
PROVIDER: 85681 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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2012-12-29 | GSE38716 | GEO
Project description:Plasma samples from 10 colonrectal cancer patients (CRCs) (including 5 stage II and 5 stage III patients) and 10 normal controls.An amount of 5 to 10 milliliters of whole blood were obtained from each participant.The plasma was obtained by centrifugation at 1200g for 10min at 4°C.To complete the removal of residual cellular components, plasma samples were recentrifuged at 12,000g for a further 10min at 4°C.A volume of 600?L of each plasma samples from CRC group or normal control group was picked out and uniformly mixed. qPCR miRNA expression profiling. Plasma samples form 10 colonrectal cancer patients(CRCs) (including 5 stage II and 5 stage III patients) and 10 normal controls were used and treated as indicated in the summary. Equal amount total RNA from each donor was pooled prior to gene expression analysis.
2012-12-29 | E-GEOD-38716 | biostudies-arrayexpress
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Project description:The elevated expression of the splicing regulator SRSF10 in metastatic colorectal cancer (CRC) stimulates the production of the pro-tumorigenic Bclaf1-L splice variant. We discovered a group of small molecules with an aminothiazole carboxamide core (GPS167, GPS192 and others) that decrease production of Bclaf1-L. While additional alternative splicing events regulated by SRSF10 are affected by GPS167/192 in HCT116 cells (e.g., in MDM4, WTAP, SLK1 and CLK1), other events are shifted in a SRSF10-independent manner (e.g., in MDM2, NAB2 and TRA2A). GPS167/192 increased the interaction of SRSF10 with the CLK1 and CLK4 kinases, leading us to show that GPS167/192 are CLK kinase inhibitors preferentially impacting the activity of SRSF10. Notably, GPS167 impairs the growth of CRC cell lines and organoids, inhibits anchorage-independent colony formation, cell migration, and promotes cytoxicity that requires SRSF10 and p53. In contrast, GPS167 only minimally affects normal colonocytes and normal colorectal organoids. Thus, GPS167 reprograms the tumorigenic activity of SRSF10 in CRC cells to elicit p53-dependent apoptosis.
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Project description:MicroRNAs are a family of 19- to 25-nucleotides noncoding small RNAs that primarily function as gene regulators. Aberrant microRNA expression has been described for several human malignancies, and this new class of small regulatory RNAs has both oncogenic and tumor suppressor functions. Despite this knowledge, there is little information regarding microRNAs in blood especially because microRNAs in blood, if exist, were thought to be digested by RNase. Recent studies, however, have revealed that microRNAs exist and escape digestion in serum and plasma. Thus, we performed microRNA microaray to obtain insight into microRNA deregulation in the plasma of a leukemia patient. Here, we have revealed that microRNA-638 (miR-638) is stably present in human plasmas, and miR-92a dramatically decreased in the plasmas of acute leukemia patients. Our data indicate that the ratio of miR-92a/miR-638 in plasma has strong potential for clinical application as a novel biomarker for detection of leukemia. Seven normal samples and two acute leukemia samples ware profiled and compared.
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Project description:The elevated expression of the splicing regulator SRSF10 in metastatic colorectal cancer (CRC) stimulates the production of the pro-tumorigenic Bclaf1-L splice variant. We discovered a group of small molecules with an aminothiazole carboxamide core (GPS167, GPS192 and others) that decrease production of Bclaf1-L. While additional alternative splicing events regulated by SRSF10 are affected by GPS167/192 in HCT116 cells (e.g., in MDM4, WTAP, SLK1 and CLK1), other events are shifted in a SRSF10-independent manner (e.g., in MDM2, NAB2 and TRA2A). GPS167/192 increased the interaction of SRSF10 with the CLK1 and CLK4 kinases, leading us to show that GPS167/192 are CLK kinase inhibitors preferentially impacting the activity of SRSF10. Notably, GPS167 impairs the growth of CRC cell lines and organoids, inhibits anchorage-independent colony formation, cell migration, and promotes cytoxicity that requires SRSF10 and p53. In contrast, GPS167 only minimally affects normal colonocytes and normal colorectal organoids. Thus, GPS167 reprograms the tumorigenic activity of SRSF10 in CRC cells to elicit p53-dependent apoptosis.
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