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

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.