SEC61G is upregulated and required for tumor progression in human kidney cancer

Meng,Hui; Jiang,Xuewen; Wang,Jian; Sang,Zunmeng; Guo,Longfei; Yin,Gang; Wang,Yu

doi:10.3892/mmr.2021.12066

SEC61G is upregulated and required for tumor progression in human kidney cancer

Authors:
- Hui Meng
- Xuewen Jiang
- Jian Wang
- Zunmeng Sang
- Longfei Guo
- Gang Yin
- Yu Wang
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Affiliations: Department of Urology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China, Department of Urology, People's Hospital of Laoling, Laoling, Shandong 253600, P.R. China, Reproductive Medicine Center, Department of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China
Published online on: April 7, 2021 https://doi.org/10.3892/mmr.2021.12066
Article Number: 427
Copyright: © Meng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Kidney cancer is a malignant tumor of the urinary system. Although the 5‑year survival rate of patients with kidney cancer has increased by ~30% in recent years due to the early detection of low‑grade tumors using more accurate diagnostic methods, the global incidence of kidney cancer continues to increase every year. Therefore, identification of novel and efficient candidate genes for predicting the prognosis of patients with kidney cancer is important. The present study aimed to investigate the role of SEC61 translocon subunit‑γ (SEC61G) in kidney cancer. The Cancer Genome Atlas database was screened to obtain the expression profile of SEC61G and identify its association with kidney cancer prognosis. Furthermore, the in vitro effect of SEC61G knockdown on kidney cancer cell proliferation, migration, invasion and apoptosis was investigated using a Cell Counting Kit‑8 assay, wound healing assay, Transwell assay and flow cytometry. The results demonstrated that compared with healthy tissues, SEC61G was upregulated in human kidney tumor tissues, which was associated with poor prognosis. In addition, SEC61G knockdown significantly inhibited kidney cancer cell proliferation, migration and invasion compared with the negative control (NC) group. Furthermore, E‑cadherin expression was significantly upregulated, and N‑cadherin and β‑catenin expression levels were significantly downregulated in SEC61G‑knockdown kidney cancer cells compared with the NC group. In addition, compared with the NC group, SEC61G knockdown significantly promoted cell apoptosis in a caspase‑dependent manner. The aforementioned results suggested that SEC61G might serve as a proto‑oncogene to promote kidney tumor progression. Therefore, the present study provided a novel candidate gene for predicting the prognosis of patients with kidney cancer.

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