http://purl.uniprot.org/citations/28339062 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/28339062 | http://www.w3.org/2000/01/rdf-schema#comment | "Colorectal cancer (CRC) has a rising morbidity worldwide and its resistance to chemotherapy has been observed in clinical treatment. Tumor suppressor p53 is well-studied in CRC, but little is known about its effects during DNA damage of CRC cells. This study was aimed at uncovering potential mechanisms of p53 regarding microRNA-374b and v-akt murine thymoma viral oncogene homolog 1 (AKT1) during DNA damage of CRC cells. CRC cells HCT116 and HT29 were transfected with p53-specific small interfering RNA (siRNA), p53 overexpression vector or miR-374b inhibitor, and then treated with 10 µM bleomycin (BLM) for 24 h to induce DNA damage. Primary (pri), precursor (pre) and mature miR-374b levels were quantified by qRT-PCR. AKT1 and p53 protein levels were detected by western blotting. Cell apoptosis changes were assessed by flow cytometry. AKT1 mRNA was detected to be induced by BLM treatment (P<0.05), but its protein level was strongly inhibited. Knockdown of p53 reversed the inhibition of AKT1 protein by BLM. Overexpression of p53 in p53-knockout HCT116 and HT29 cells upregulated the AKT1 regulator miR-374b (P<0.05), and knockdown of p53 reversed the induction of miR-374b by BLM. qRT-PCR suggested that besides mature miR-374b, p53 could also promote pre-miR-374b level (P<0.05), rather than pri-miR-374b. Moreover, inhibition on miR-374b relieved the suppressed AKT1 protein, and reduced cell apoptosis induced by BLM. These data depict the p53/miR-374b/AKT1 signaling that may regulate BLM-induced apoptosis in CRC cells, thus facilitating to improve the outcome of chemotherapy in CRC."xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.org/dc/terms/identifier | "doi:10.3892/ijo.2017.3922"xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/author | "Cao Y."xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/author | "Gong H."xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/author | "Han G."xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/author | "Pan Y."xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/author | "Zhang Y."xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/author | "You Q."xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/name | "Int J Oncol"xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/pages | "1785-1791"xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/title | "p53/microRNA-374b/AKT1 regulates colorectal cancer cell apoptosis in response to DNA damage."xsd:string |
http://purl.uniprot.org/citations/28339062 | http://purl.uniprot.org/core/volume | "50"xsd:string |
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