| Summary: | EndoG influences mitochondrial DNA replication and is involved in somatic cell proliferation. Here, we investigated the effect of <i>ENDOG/Endog</i> expression on proliferation in different tumor models. Noteworthy, <i>ENDOG</i> deficiency reduced proliferation of endometrial tumor cells expressing low PTEN/high <i>p</i>-AKT levels, and <i>Endog</i> deletion blunted the growth of PTEN-deficient 3D endometrial cultures. Furthermore, <i>ENDOG</i> silencing reduced proliferation of follicular thyroid carcinoma and glioblastoma cell lines with high <i>p</i>-AKT expression. High <i>ENDOG</i> expression was associated with a short time to treatment in a cohort of patients with chronic lymphocytic leukemia (CLL), a B-cell lymphoid neoplasm with activation of PI3K/AKT. This clinical impact was observed in the less aggressive CLL subtype with mutated IGHV in which high <i>ENDOG</i> and low <i>PTEN</i> levels were associated with worse outcome. In summary, our results show that reducing <i>ENDOG</i> expression hinders growth of some tumors characterized by low PTEN activity and high <i>p</i>-AKT expression and that <i>ENDOG</i> has prognostic value for some cancer types.
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