Cell cycle restoration after DNA damage in cancer cells.

<p>SCR or SLD5 siRNA transfected B16 (<b>A, B</b>) or Colon26 (<b>C, D</b>) cells were treated with DMSO (<b>A,</b><b>C</b>) or etoposide (<b>B,</b><b>D</b>) as indicated in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0110483#pone-0110483-g006" target="_blank">Figure 6</a> and the same number of living cells as indicated were cultured with fresh medium for 72 h. Cell numbers were recorded. Data represent the mean ± SD.*, <i>P</i><0.05 (n = 3).</p

Attenuation of SLD5 expression induces marked DNA damage in cancer cells.

<p>Western blot analysis of γ-H2AX expression in SCR or SLD5 siRNA-transfected B16 (<b>A,</b><b>B</b>) or Colon26 (<b>C,</b><b>D</b>) cells after treatment with etoposide (ETO) or control vehicle (DMSO). β-actin was the internal control. Data were quantitatively evaluated based on densitometric analysis (<b>B</b>, <b>D</b>). Results are fold-change compared with the level seen in SCR siRNA-treated B16 cells (<b>B</b>) or Colon26 cells (<b>D</b>), respectively. Data represent the mean ± SD. *, <i>P</i><0.05 (n = 3).</p

Attenuation of SLD5 expression results in marked DNA damage in MEFs.

<p>(<b>A</b>) Western blot analysis of SLD5 expression in WT and SLD5^+/− MEFs. β-actin was the internal control. (<b>B</b>) Quantitative evaluation of SLD5 expression as revealed in (<b>A</b>) based on densitometric analysis. Results are represented as fold-change compared with the level seen in WT MEFs. Data represent the mean ± SD. *, <i>P</i><0.05 (n = 3). (<b>C</b>) Western blot analysis of γ-H2AX expression in WT and SLD5^+/− MEFs after treatment with etoposide (ETO) or control vehicle (DMSO). β-actin was the internal control. (<b>D</b>) Quantitative evaluation of γ-H2AX expression as revealed in (<b>C</b>). Results are fold-changes compared with the level seen in WT MEFs treated with DMSO. Data represent the mean ± SD. *, <i>P</i><0.05 (n = 3).</p

Impaired cell cycle restoration after DNA damage in SLD5^+/− MEFs.

<p>MEFs were treated with DMSO (<b>A</b>) or etoposide (<b>B</b>) as indicated in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0110483#pone-0110483-g002" target="_blank">Figure 2</a> and the same number of living cells as indicated were cultured with fresh medium for 72 h. Cells were counted at the indicated time. Data represent the mean ± SD. *, <i>P</i><0.05 (n = 3).</p

Delayed and prolonged Rad51 expression after DNA damage by etoposide in SLD5^+/− MEFs.

<p>(<b>A</b>) Western blot analysis of Rad51 expression in WT and SLD5^+/− MEFs. β-actin was the internal control. MEFs were treated with etoposide for 12 h (−12∼0) and lysed at the indicated times. (<b>B</b>) Quantitative evaluation of Rad51 expression as revealed in (<b>A</b>) based on densitometric analysis. Results are fold-change compared with the level seen in WT MEFs before treatment with etoposide. Data represent the mean ± SD.*, <i>P</i><0.05 (n = 3).</p