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

被引：0
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作者：
Yi Sang
Jianjun Tang
Siwei Li
Liping Li
XiaoFeng Tang
Chun Cheng
Yanqin Luo
Xia Qian
Liang-Ming Deng
Lijuan Liu
Xiao-Bin Lv
机构：
[1] Nanchang Key Laboratory of Cancer Pathogenesis and Translational Research,Department of Gastroenterology
[2] Center Laboratory,Department of Radiation Oncology
[3] the Third Affiliated Hospital,Department of Medicine
[4] Nanchang University,Department of pharmacy
[5] Cancer Hospital of Jiangxi Province,undefined
[6] the Affiliated Hospital of Guilin Medical University,undefined
[7] GaomingHeshui Hospital,undefined
[8] Cancer Hospital of Jiangxi Province,undefined
来源：
Scientific Reports | / 6卷
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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 p16INK4A. Moreover, we showed that PANDAR impacted p16INK4A expression by regulating the recruitment Bmi1 to p16INK4A 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/p16INK4A axis could serve as novel targets for breast cancer therapy.
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