| http://purl.uniprot.org/citations/31868942 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/31868942 | http://www.w3.org/2000/01/rdf-schema#comment | "Oral squamous cell carcinoma (OSCC) is one of the most common types of head and neck neoplasm. Down-regulation of hsa-microRNA-378 (miR-378) has been proved in OSCC tissues, suggesting that miR-378 might play crucial roles in the progression of OSCC. The present study aimed to evaluate the effect of miR-378-3p/5p on the proliferation and apoptosis of OSCC in vitro and in vivo. According to the results, lentivirus-mediated overexpression of miR-378 lowered the colony formation efficiency, blocked cell cycle progression, and decreased the percentage of Ki-67 positive cells, whereas knockdown of miR-378-3p/5p led to the opposite results. Furthermore, the apoptosis of OSCC cells was induced by the overexpression of miR-378 as evidenced by decreasing Bcl-2/Bax ratio, increasing cleaved caspase-9, cleaved caspase-3, and cleaved PARP levels, and promoting the release of cytochrome c into the cytoplasm. However, the above results were reversed by miR-378-3p/5p silencing. In addition, the overexpression of miR-378 inhibited the activation of PI3K/AKT signalling pathway. Conversely, miR-378-3p/5p knockdown resulted in the inactivation of PI3K/AKT signalling pathway. Mechanically, we validated that miR-378-3p/5p could target kallikrein-related peptidase 4 (KLK4), and enforced overexpression of KLK4 counteracted miR-378 overexpression-induced apoptosis. Finally, tumourigenesis in nude mice was suppressed by the overexpression of miR-378, which was promoted by miR-378-3p/5p silencing. Taken together, these results suggest that miR-378 may be a potential target in the diagnoses and treatment of OSCC."xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.org/dc/terms/identifier | "doi:10.1111/1440-1681.13235"xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/author | "Cui Z."xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/author | "Huang L."xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/author | "Liu Q."xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/author | "Li Q."xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/author | "Wang H."xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/author | "Bao X."xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/author | "Jiao K."xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/name | "Clin Exp Pharmacol Physiol"xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/pages | "713-724"xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/title | "MicroRNA-378-3p/5p represses proliferation and induces apoptosis of oral squamous carcinoma cells via targeting KLK4."xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://purl.uniprot.org/core/volume | "47"xsd:string |
| http://purl.uniprot.org/citations/31868942 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/31868942 |
| http://purl.uniprot.org/citations/31868942 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/31868942 |
| http://purl.uniprot.org/uniprot/#_A0A0C4DFQ5-mappedCitation-31868942 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/31868942 |
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| http://purl.uniprot.org/uniprot/#_Q96JE0-mappedCitation-31868942 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/31868942 |