PMID- 28298621
OWN - NLM
STAT- MEDLINE
DCOM- 20170621
LR  - 20190606
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 23
DP  - 2017 Mar 16
TI  - Silencing nc886, a Non-Coding RNA, Induces Apoptosis of Human Endometrial Cancer 
      Cells-1A In Vitro.
PG  - 1317-1324
AB  - BACKGROUND The role that nc886, a non-coding microRNA, plays in human endometrial 
      cancer is unknown. The present study aimed to describe the functional role of 
      nc886 in human endometrial cancer-1A (HEC-1A) cell line, which may provide 
      another target for human endometrial cancer treatment. MATERIAL AND METHODS The 
      expression levels of nv886 in normal human endometrial tissue and the early phase 
      and late phase of human endometrial cancer tissues were determined and compared 
      by fluorescence in situ hybridization (FISH). Small interference RNA (siRNA) was 
      used to inhibit nc886, and cell proliferation was evaluated with the MTT test. 
      mRNA levels of PKR, NF-kappaB, vascular endothelial growth factor (VEGF), and 
      caspase-3 were determined against glyceraldehyde 3-phosphate dehydrogenase (GAPDH 
      between the HEC-1A control group and the silenced group (nc886 silenced with 
      siRNA) by real-time reverse transcription polymerase chain reaction (RT-PCR). The 
      protein levels of PKR (total and phosphorylated form), NF-kappaB, VEGF, and caspase-3 
      were determined against GAPDH by Western blotting, and cell apoptosis was 
      determined by flow cytometry. RESULTS Our results indicated that a higher level 
      of nc886 was expressed in the late phase of human endometrial cancer tissue, less 
      than in the early phase but still higher than in normal human endometrial tissue. 
      After nc886 was silenced, protein levels of p-PKR (phosphorylated PKR) and 
      caspase-3 were increased, whereas NF-kappaB and VEGF were decreased. CONCLUSIONS The 
      rate of apoptosis in the silenced group was increased and the rate of cell 
      proliferation was slower in comparison to the control.
FAU - Hu, Zhuoying
AU  - Hu Z
AD  - Department of Obstetrics and Gynecology, The 1st Affiliated Hospital of Chongqing 
      Medical University, Chongqing, China (mainland).
FAU - Zhang, Hongyu
AU  - Zhang H
AD  - Department of General Surgery, The 1st Affiliated Hospital of Chongqing Medical 
      University, Chongqing, China (mainland).
FAU - Tang, Liangdan
AU  - Tang L
AD  - Department of Obstetrics and Gynecology, The 1st Affiliated Hospital of Chongqing 
      Medical University, Chongqing, China (mainland).
FAU - Lou, Meng
AU  - Lou M
AD  - Department of Obstetrics and Gynecology, The 1st Affiliated Hospital of Chongqing 
      Medical University, Chongqing, China (mainland).
FAU - Geng, Yanqing
AU  - Geng Y
AD  - Department of Obstetrics and Gynecology, The 1st Affiliated Hospital of Chongqing 
      Medical University, Chongqing, China (mainland).
LA  - eng
PT  - Journal Article
DEP - 20170316
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (MIRN886 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Apoptosis/genetics
MH  - Caspase 3/metabolism
MH  - Cell Line, Tumor
MH  - Cell Proliferation/genetics
MH  - Endometrial Neoplasms/*genetics/metabolism/*therapy
MH  - Endometrial Stromal Tumors/*genetics/metabolism/*therapy
MH  - Female
MH  - Gene Silencing
MH  - HeLa Cells
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - MicroRNAs/*genetics/metabolism
MH  - NF-kappa B/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - RNA, Small Interfering/administration & dosage/genetics
MH  - Transfection
PMC - PMC5365049
EDAT- 2017/03/17 06:00
MHDA- 2017/06/22 06:00
PMCR- 2017/03/16
CRDT- 2017/03/17 06:00
PHST- 2017/03/17 06:00 [entrez]
PHST- 2017/03/17 06:00 [pubmed]
PHST- 2017/06/22 06:00 [medline]
PHST- 2017/03/16 00:00 [pmc-release]
AID - 900320 [pii]
AID - 10.12659/msm.900320 [doi]
PST - epublish
SO  - Med Sci Monit. 2017 Mar 16;23:1317-1324. doi: 10.12659/msm.900320.