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16 March 2017 : Laboratory Research  

Silencing nc886, a Non-Coding RNA, Induces Apoptosis of Human Endometrial Cancer Cells-1A In Vitro

Zhuoying Hu1BC, Hongyu Zhang2CD, Liangdan Tang1AB*, Meng Lou1DE, Yanqing Geng1EF

DOI: 10.12659/MSM.900320

Med Sci Monit 2017; 23:1317-1324

Abstract

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-κB, 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-κB, 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-κB 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.

Keywords: Caspase 3, Endometrial Stromal Tumors, Uterine Diseases

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750