Silencing of ABCG2 by MicroRNA-3163 Inhibits Multidrug Resistance in Retinoblastoma Cancer Stem Cells.
10.3346/jkms.2016.31.6.836
- Author:
Ming JIA
1
;
Zhenhua WEI
;
Peng LIU
;
Xiaoli ZHAO
Author Information
1. Department of Ophthalmology, Linzi District People's Hospital, Zibo City, Shandong Province, P. R. China. jiaming_20150401@163.com
- Publication Type:Original Article
- Keywords:
Retinoblastoma;
RCSCs;
ABCG2;
miR-3163
- MeSH:
3' Untranslated Regions;
ATP Binding Cassette Transporter, Sub-Family G, Member 2/antagonists & inhibitors/genetics/*metabolism;
Antagomirs/metabolism;
Antineoplastic Agents/toxicity;
Apoptosis/drug effects;
Base Sequence;
Cell Line, Tumor;
Cell Proliferation/drug effects;
Drug Resistance, Neoplasm/drug effects;
Gene Silencing;
Humans;
MicroRNAs/antagonists & inhibitors/genetics/*metabolism;
Neoplasm Proteins/antagonists & inhibitors/genetics/*metabolism;
Neoplastic Stem Cells/*metabolism;
Retinoblastoma/metabolism/pathology;
Sequence Alignment;
Transfection
- From:Journal of Korean Medical Science
2016;31(6):836-842
- CountryRepublic of Korea
- Language:English
-
Abstract:
To investigate the function and regulation mechanism of ATP-binding cassette, subfamily G, member 2 (ABCG2) in retinoblastoma cancer stem cells (RCSCs), a long-term culture of RCSCs from WERI-Rb1 cell line was successfully established based on the high expression level of ABCG2 on the surface of RCSCs. To further explore the molecular mechanism of ABCG2 on RCSCs, a microRNA that specifically targets ABCG2 was predicted. Subsequently, miR-3163 was selected and confirmed as the ABCG2-regulating microRNA. Overexpression of miR-3163 led to a significant decrease in ABCG2 expression. Additionally, ABCG2 loss-of-function induced anti-proliferation and apoptosis-promoting functions in RCSCs, and multidrug resistance to cisplatin, carboplatin, vincristine, doxorubicin, and etoposide was greatly improved in these cells. Our data suggest that miR-3163 has a significant impact on ABCG2 expression and can influence proliferation, apoptosis, and drug resistance in RCSCs. This work may provide new therapeutic targets for retinoblastoma.
