Gelsolin inhibits the proliferation and invasion of the 786-0 clear cell renal cell carcinoma cell line in vitro.

Xiaoling Zhu,Xiaoming Jin,Qinggang Meng,Limin Cai

doi:10.3892/mmr.2015.4313

Xiaoling Zhu, Xiaoming Jin + Show 2 more

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https://doi.org/10.3892/mmr.2015.4313

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Abstract

The aim of the present study was to investigate the effect of gelsolin (GSN) on the proliferation and invasion of the 786-0 clear cell renal cell carcinoma (ccRCC) cell line in vitro. A GSN overexpression lentiviral vector was constructed and transfected into 786‑0 ccRCC cells in vitro. A 3-(4,5-dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide (MTT) assay was conducted to detect the effect of GSN on the proliferation and adhesion ability of the 786‑0 ccRCC cells, and a Transwell invasion assay was used to determine the effect of GSN on the invasion of 786‑0 ccRCC cells. In addition, the expression levels of invasion‑associated proteins, matrix metalloproteinase (MMP)2, MMP9 and E‑cadherin were analyzed by ELISA and western blotting. The MTT assay demonstrated a significantly lower optical density value for the 786‑0/GSN cells compared with that of the 786‑0/green fluorescent protein (GFP) and 786‑0 cells following 24‑ and 48‑h culture (P<0.05). The mean penetration rate of the 786‑0/GSN cells was significantly lower than that of the 786‑0/GFP and 786‑0 cells (P<0.05) according to the Transwell invasion assay. The expression levels of MMP2 and MMP9 were significantly decreased in the 786‑0/GSN cells, when compared with the 786‑0/GFP and 786‑0 cells following a 48‑h transfection, according to ELISA (P<0.001). Furthermore, in the 786‑0/GSN cells, the expression levels of MMP2 and MMP9 were markedly decreased, while the expression of E‑cadherin was markedly increased. Thus, the overexpression of GSN may inhibit the proliferation, adhesion ability and invasion of 786‑0 ccRCC cells. Additionally, GSN downregulated the expression of MMP2 and MMP9, and upregulated the expression of E‑cadherin in the 786‑0 ccRCC cells, which may have suppressed the invasion ability of the 786-0 ccRCC cells.

Highlights

Renal cell carcinoma (RCC) arises from the renal tubular epithelium and accounts for 2‐3% of all adult malignancies in the USA [1]
Since advanced clear cell RCC (ccRCC) is highly resistant to chemotherapy and cytotoxic therapeutic agents, one‐third of patients will experience recurrence following resection of the tumor [6]
Western blot analysis demonstrated that the expression level of GSN was markedly increased in the 786‐0/GSN cells, when compared with the 786‐0/green fluorescent protein (GFP) and 786‐0 cells (Table II and Fig. 3)

Summary

Introduction

Renal cell carcinoma (RCC) arises from the renal tubular epithelium and accounts for 2‐3% of all adult malignancies in the USA [1]. Four types of RCC have been clinically characterized, with 85% of cases of adult RCC being clear cell RCC (ccRCC), while the other 15% are the papillary, chromophobe and oncocytic types [1]. The incidence of ccRCC is steadily increasing by 2.5% per year, and >64,700 new cases and 13,500 mortalities were reported in 2012 [5]. Since advanced ccRCC is highly resistant to chemotherapy and cytotoxic therapeutic agents, one‐third of patients will experience recurrence following resection of the tumor [6]. The factors involved in disease progression and metastasis provide molecular targets to facilitate the development of effective therapeutic strategies

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