TRIM24 siRNA induced cell apoptosis and reduced cell viability in human nasopharyngeal carcinoma cells

Wang,Peng; Shen,Na; Liu,Danzheng; Ning,Xianhui; Wu,Daquan; Huang,Xinsheng

doi:10.3892/mmr.2018.8946

TRIM24 siRNA induced cell apoptosis and reduced cell viability in human nasopharyngeal carcinoma cells

Authors:
- Peng Wang
- Na Shen
- Danzheng Liu
- Xianhui Ning
- Daquan Wu
- Xinsheng Huang
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Affiliations: Department of Otolaryngology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China
Published online on: May 2, 2018 https://doi.org/10.3892/mmr.2018.8946
Pages: 369-376

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Abstract

Nasopharyngeal carcinoma (NPC) is a common cancer occurring primarily in East Asia and Africa. The high rate of recurrence and metastasis of NPC continuously endangers the health of patients. The present study aimed to identify the underlying mechanisms involved in the progression of NPC and provide experimental basis to develop a novel and efficient agent against NPC. The present study measured the expression level of tripartite motif containing 24 (TRIM24) in tumor tissues from NPC patients using reverse transcription quantitative polymerase chain reaction. Subsequently, Cell Counting kit‑8 and flow cytometry were used to detect the cell proliferation and apoptosis of NPC cell lines HONE1 and CNE1 cells where the TRIM24 gene was knocked‑down with small interfering RNA (siRNA). Further, caspase kits and western blot analysis were used to detect the expression of apoptosis and angiogenesis‑associated proteins. The present study detected a higher expression level of TRIM24 in tumor tissues and NPC cell lines and lower cell viability and higher apoptotic rate were observed when TRIM24 was silenced. Meanwhile, upregulated caspase‑3 and caspase‑9 indicated induced cell apoptosis in HONE1 and CNE1 cells following the treatment with TRIM24 siRNA. Additionally, the downregulated expression level of vascular endothelial growth factor (VEGF) and VEGF receptor 2 suggested inhibited angiogenesis of NPC cells. Additionally, the reduced levels of janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) indicated a blocked JAK2/STAT3 signaling pathway. However, there was no direct evidence that inactivation of the JAK2/STAT3 signaling pathway was involved in regulation of siTRIM24, these results suggested that TRIM24 has an important role in the growth of NPC. Additionally, silenced TRIM24 may lead to inhibited cell proliferation and induced cell apoptosis in NPC cells. The limitation of this study was that HONE1, CNE1 and CNE2 cells may have been contaminated with other cells. Further experiments with validated NPC cells may be needed.

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