LncRNA PANDAR regulates the G1/S transition of breast cancer cells by suppressing p16INK4A expression

被引：58
|
作者：
Sang, Yi [1 ]
Tang, Jianjun [2 ]
Li, Siwei [3 ]
Li, Liping [1 ]
Tang, XiaoFeng [1 ]
Cheng, Chun [1 ]
Luo, Yanqin [1 ]
Qian, Xia [1 ]
Deng, Liang-Ming [4 ]
Liu, Lijuan [5 ]
Lv, Xiao-Bin [1 ]
机构：
[1] Nanchang Univ, Affiliated Hosp 3, Ctr Lab, Nanchang Key Lab Canc Pathogenesis & Translat Res, Nanchang, Peoples R China
[2] Canc Hosp Jiangxi Prov, Dept Gastroenterol, Nanchang, Peoples R China
[3] Guilin Med Univ, Affiliated Hosp, Dept Radiat Oncol, Guilin, Peoples R China
[4] GaomingHeshui Hosp, Dept Med, Foshan, Peoples R China
[5] Canc Hosp Jiangxi Prov, Dept Pharm, Nanchang, Peoples R China
来源：
SCIENTIFIC REPORTS | 2016年 / 6卷
关键词：
LONG NONCODING RNAS; MEDIATED DEGRADATION; POOR-PROGNOSIS; METASTASIS; APOPTOSIS; IDENTIFICATION; TUMORIGENESIS; MICRORNAS; STABILITY; GROWTH;
D O I：
10.1038/srep22366
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
It has been reported that lncRNA PANDAR (promoter of CDKN1A antisense DNA damage-activated RNA) is induced as a result of DNA damage, and it regulates the reparation of DNA damage. In this study, we investigated the role of lncRNA PANDAR in the progression of breast cancer and found that PANDAR was up-regulated in breast cancer tissues and cell lines. The knockdown of PANDAR suppresses G1/S transition of breast cancer cells. We demonstrated mechanistically that the regulation of G1/S transition by PANDAR was partly due to the transcriptional modulation of p16(INK4A). Moreover, we showed that PANDAR impacted p16(INK4A) expression by regulating the recruitment Bmi1 to p16(INK4A) promoter. To our knowledge, this is the first study which showed the functional roles and mechanisms of PANDAR in regulating the progression of breast cancer. The PANDAR/Bmi1/p16(INK4A) axis could serve as novel targets for breast cancer therapy.
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页数：10
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