Expression of B cell-specific Moloney murine leukemia virus integration site 1 in vulvar squamous cell carcinoma and its effect on the biological behavior of A-431 cells
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- Published online on: September 25, 2015 https://doi.org/10.3892/ol.2015.3754
- Pages: 3369-3376
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Copyright: © Bai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
The aim of the present study was to investigate the expression of B cell‑specific Moloney murine leukemia virus integration site 1 (BMI‑1) in vulvar squamous cell carcinoma (VSCC) and vulvar intraepithelial neoplasia (VIN). Furthermore, the present study investigated the effects of BMI‑1 expression on the biological behavior of A‑431 human epidermoid carcinoma cells. BMI‑1 expression in human VSCC and VIN tissues was detected using immunohistochemistry. Subsequently, BMI‑1 expression was silenced in A‑431 cells using small interfering RNA (siRNA), and BMI‑1 expression was detected using reverse transcription‑quantitative polymerase chain reaction and western blotting. The effects of BMI‑1 silencing on cell proliferation, apoptosis and invasive ability were determined using an MTT assay, Annexin V‑fluorescein isothiocyanate/propidium iodide double‑labeling experiment and Transwell assay, respectively. The expression rate of BMI‑1 in normal vulvar, VIN and VSCC tissues was 0.0, 25.0 and 68.0% respectively, demonstrating an increasing trend in the severity of the disease. BMI‑1 overexpression was found not to correlate with age, pathological stage, lymph node metastasis or degree of differentiation (P>0.05). BMI‑1 siRNA transfection effectively inhibited BMI‑1 messenger RNA and protein expression in A‑431 cells. The mean rate of apoptosis promotion and proliferation inhibition in the most effectively silenced group were 20.19 and 46.82%, respectively, which was significantly higher than that of the cells in the blank and control siRNA groups (P<0.05). The number of invading cells was decreased in the most effectively silenced group compared with that of the blank and control siRNA groups. Abnormal expression of BMI‑1 was also detected in VIN and VSCC tissues, and targeting of BMI‑1 with siRNA was able to successfully silence BMI‑1 expression in A‑431 cells. Silencing of BMI‑1 promoted apoptosis and inhibited the invasive abilities of A‑431 cells in vitro.
