http://rdf.ncbi.nlm.nih.gov/pubchem/patent/KR-102181813-B1
Outgoing Links
Predicate | Object |
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classificationCPCAdditional | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K2039-505 |
classificationCPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-506 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K48-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K39-39558 |
classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-506 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K48-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K39-395 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K39-00 |
filingDate | 2019-10-31-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
grantDate | 2020-11-24-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
publicationDate | 2020-11-24-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
publicationNumber | KR-102181813-B1 |
titleOfInvention | Therapeutic compositions for breast cancer containing protein kinase D1 |
abstract | One of the characteristics of human breast cancer is cancer stem cellity, which is characterized by self-modifying ability and drug resistance. Protein kinase D1 (PRKD1) functions as a major regulator of many cellular processes and is downregulated in invasive breast cancer cells. The present invention revealed that PRKD1 is upregulated in MCF-7-ADR human breast cancer cells with drug resistance characteristics. In addition, the present inventors revealed that PRKD1 expression is negatively regulated by binding of miR-34a to PRKD1 3'-UTR. PRKD1 expression in MCF-7-ADR cells increased after performing tumor cell formation assay. The present inventors also revealed that the reduction of PRKD1 by translocation miR-34a expression or PRKD1 siRNA treatment in breast cancer stem cells inhibits the self-remodeling ability, furthermore, PRKD1 inhibitor CRT0066101 reduces phosphorylated PKD/PKCμ, GSK3/β- It was confirmed that breast cancer stem cells were inhibited through catenin signaling. In MCF-7-ADR cells, PRKD1 inhibition also influenced the onset of apoptosis. Tumor growth, proliferation, and induced apoptosis were inhibited in tumors of nude mice treated with miR-34a or CRT0066101. These results demonstrate that PRKD1 regulation, a target of the novel miR-34a, will contribute to overcoming cancer cell stemness and drug resistance in human breast cancer. |
isCitedBy | http://rdf.ncbi.nlm.nih.gov/pubchem/patent/KR-20230007123-A |
priorityDate | 2019-10-31-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
type | http://data.epo.org/linked-data/def/patent/Publication |
Incoming Links
Total number of triples: 747.