Title : Knockdown Of lncRNA NCK-AS1 Regulates Cisplatin Resistance Through Modulating miR-137 In Osteosarcoma Cells.

Pub. Date : 2019

PMID : 31908475






6 Functional Relationships(s)
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1 The present study aimed to explore whether lncRNA NCK-AS1 could affect the cisplatin (DDP) resistance in human osteosarcoma cell and the underlying molecular mechanism. 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate prostaglandin D2 receptor Homo sapiens
2 Results: The results revealed that NCK1-AS1 was significantly upregulated in osteosarcoma cells, as well as in DDP-resistant osteosarcoma cells. 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate prostaglandin D2 receptor Homo sapiens
3 NCK1-AS1 silence inhibited the proliferation, migration and invasion of osteosarcoma cells, whereas enhanced the sensitivity of osteosarcoma cells to DDP. 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate prostaglandin D2 receptor Homo sapiens
4 Most importantly, miR-137 overexpression enhanced the sensitivity of osteosarcoma cells to DDP, and high expression of NCK1-AS1 reversed the influences of miR-137 overexpression on DDP-resistant cells. 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate prostaglandin D2 receptor Homo sapiens
5 Conclusion: In short, NCK1-AS1 knockdown enhanced DDP sensitivity of osteosarcoma cells by regulating miR-137, which may be a novel potential target for anti-DDP resistance in human osteosarcoma. 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate prostaglandin D2 receptor Homo sapiens
6 Conclusion: In short, NCK1-AS1 knockdown enhanced DDP sensitivity of osteosarcoma cells by regulating miR-137, which may be a novel potential target for anti-DDP resistance in human osteosarcoma. 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate prostaglandin D2 receptor Homo sapiens