SHCBP1 regulates apoptosis in lung cancer cells through phosphatase and tensin homolog

Wang,Fei; Li,Yi; Zhang,Zhe; Wang,Jingxin; Wang,Jinghao

doi:10.3892/ol.2019.10520

SHCBP1 regulates apoptosis in lung cancer cells through phosphatase and tensin homolog

Authors:
- Fei Wang
- Yi Li
- Zhe Zhang
- Jingxin Wang
- Jinghao Wang
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Affiliations: Department of Thoracic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China, Department of Neurology, Harbin Children's Hospital, Harbin, Heilongjiang 150086, P.R. China, Department of Pharmacy, Hongqi Hospital of Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China, Department of Pharmacy, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong 510630, P.R. China
Published online on: June 24, 2019 https://doi.org/10.3892/ol.2019.10520
Pages: 1888-1894
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Src homologous and collagen (SHC) SH2‑binding protein 1 (SHCBP1) is a member of the SHC family, and is overexpressed in numerous types of cancer. In addition, apoptosis serves an important role in the development of cancer. The purpose of this study was to examine the effect of SHCBP1 on apoptosis and its potential underlying mechanism in lung cancer cells. Apoptosis was detected by flow cytometry and caspase‑3 activity analysis. The expression levels of SHCBP1 and phosphatase and tensin homolog (PTEN) were detected by western blot analysis and reverse transcription‑quantitative polymerase chain reaction. Cell viability was determined by MTT assay. The results indicated that SHCBP1 was increased in lung cancer cell lines and lung cancer tissues compared with in normal lung cell lines and tissues. The apoptosis of lung cancer cells was significantly increased by SHCBP1 small interfering RNA (siRNA), as indicated by the increased number of apoptotic cells and enhanced caspase‑3 activity. In addition, it was demonstrated that PTEN expression was modulated by SHCBP1 knockdown; silencing of SHCBP1 expression led to a significant increase in PTEN expression. Furthermore, inhibition of PTEN by siRNA reversed the increase in apoptosis induced by SHCBP1 siRNA. These results suggested that SHCBP1 may be upregulated in lung cancer and it may serve a key role in the apoptosis of lung cancer cells; this effect was associated with the expression of PTEN.

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