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As part of the  Reproducibility Project: Cancer Biology  we published a Registered Report (Khan et al., 2015), that described how we intended to replicate selected experiments from the paper "A coding-independent function of gene and pseudogene mRNAs regulates tumour biology" (Poliseno et al., 2010). Here we report the results. We found  PTEN  depletion in the prostate cancer cell line DU145 did not detectably impact expression of the corresponding pseudogene  PTENP1 . Similarly, depletion of  PTENP1  did not impact  PTEN  mRNA levels. The original study reported  PTEN  or  PTENP1  depletion statistically reduced the corresponding pseudogene or gene (Figure 2G; Poliseno et al., 2010).  PTEN  and/or  PTENP1  depletion in DU145 cells decreased PTEN protein expression, which was similar to the original study (Figure 2H; Poliseno et al., 2010). Further, depletion of  PTEN  and/or  PTENP1  increased DU145 proliferation compared to non-targeting siRNA, which was in the same direction as the original study (Figure 2F; Poliseno et al., 2010), but not statistically significant. We found  PTEN  3'UTR overexpression in DU145 cells did not impact  PTENP1  expression, while the original study reported  PTEN  3'UTR increased  PTENP1  levels (Figure 4A; Poliseno et al., 2010). Overexpression of  PTEN  3'UTR also statistically decreased DU145 proliferation compared to controls, which was similar to the findings reported in the original study (Figure 4A; Poliseno et al., 2010). Differences between the original study and this replication attempt, such as level of knockdown efficiency and cellular confluence, are factors that might have influenced the results. Finally, where possible, we report meta-analyses for each result.

Replication Study: A coding-independent function of gene and pseudogene mRNAs regulates tumour biology