Inhibition of FOXQ1 induces apoptosis and suppresses proliferation in prostate cancer cells by controlling BCL11A/MDM2 expression.

Abstract

Forkhead boxQ1 (FOXQ1) has been recognized as an oncogene that is overexpressed in different cancers, and several studies have shown that FOXQ1 is related to apoptosis and proliferation in many cancer types. However, the role and the molecular mechanism of FOXQ1 in prostate cancer remains unclear. In this study, we aimed to explore the role of FOXQ1 in regulating cell apoptosis, proliferation and invasion in prostate cancer and the underlying mechanism. We found that FOXQ1 was highly expressed in the prostate cancer tissues and cell lines. In our FOXQ1 loss-of-function experiments, the data indicate that the expression of BCL11A and MDM2 was significantly downregulated, prostate cancer cell proliferation and invasion were markedly suppressed, and apoptosis was significantly induced. Moreover, overexpression of BCL11A obviously reversed the effect of FOXQ1 inhibition on apoptosis, proliferation and invasion of prostate cancer cells. In addition, BCL11A overexpression also abrogated the inhibitory effect of FOXQ1 suppression on MDM2 expression. Taken together, our study suggests that FOXQ1 regulates prostate cancer cell proliferation and apoptosis by regulating BCL11A/MDM2 expression and indicates that FOXQ1 may serve as a potential therapeutic target for prostate cancer.