Effect of ulinastatin on the expression and distribution of high mobility group box 1 in human colon carcinoma cells in vitro

Wang,Yunhua; Tao,Tao; Dong,Yinv; Zhang,Jing; Qin,Zaisheng

doi:10.3892/mmr.2014.2921

Effect of ulinastatin on the expression and distribution of high mobility group box 1 in human colon carcinoma cells in vitro

Authors:
- Yunhua Wang
- Tao Tao
- Yinv Dong
- Jing Zhang
- Zaisheng Qin
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Affiliations: Department of Anesthesiology, The First People's Hospital of Foshan and Foshan Hospital of Sun Yat‑Sen University, Foshan, Guangdong 528000, P.R. China, Department of Anesthesiology, Nanfang Hospital of Southern Medical University, Guangzhou, Guangdong 510515, P.R. China
Published online on: November 11, 2014 https://doi.org/10.3892/mmr.2014.2921
Pages: 2041-2047

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Abstract

The aim of the present study was to investigate the in vitro effects of ulinastatin (UTI) on the proliferation, invasion, apoptosis, expression and distribution of high mobility group box 1 (HMGB1) and the expression of nuclear factor κB (NF‑κB) in human colon carcinoma LoVo cells. The cells were divided into control (untreated), UTI1 (400 U/ml UTI), UTI2 (800 U/ml UTI) and UTI3 (1,600 U/ml UTI) groups. The cell proliferation, invasion, apoptosis and the gene and protein expression of HMGB1 and NF‑κB were detected using a tetrazolium assay, Transwell cell invasion assays, a caspase‑3 activity assay, western blot analysis and reverse transcription quantitative polymerase chain reaction, respectively. The distribution of HMGB1 was detected using immunofluorescence. LoVo cell proilferation decreased the most in the UTI3 group followed, in order, by the UTI2, UTI1 and control groups. UTI inhibited invasion in LoVo cells and the inhibitory effect was enhanced as the UTI concentration increased. The activity of caspase‑3 increased the least in the control group followed, in order, by the UTI1, UTI2 and UTI3 groups. UTI inhibited the expression of HMGB1 and NF‑κB, and decreased the cytoplasmic distribution of HMGB1. Thus, UTI inhibited LoVo cell proliferation and induced LoVo cell apoptosis, the mechanism of which may be associated with a decreased in the expression of HMGB1 and NF‑κB, and the cytoplasmic distribution of HMGB1.

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