Regulation of autophagy by oncogene DJ1 via the JNK signaling pathway in human ovarian cancer cells

This study investigated the regulatory role of the oncogene DJ1 in autophagy through the c-Jun N-terminal kinase (JNK) signaling pathway in human ovarian cancer SKOV3 cells. Stable transfection with DJ1-silencing and DJ1-overexpression vectors was performed in SKOV3 cells. Expression levels of autophagy-related proteins, including Beclin1, P62, and LC3, were assessed using quantitative reverse transcription polymerase chain reaction and western blotting. Autophagolysosome formation was evaluated via immunofluorescence, and phosphorylated JNK levels were assessed through western blotting. These assessments were repeated following treatment with a specific JNK pathway inhibitor. DJ1 silencing was associated with decreased Beclin1 and P62 expression, increased LC3 expression, enhanced autophagolysosome formation, and reduced JNK phosphorylation. In contrast, DJ1 overexpression led to increased Beclin1 and P62 expression, decreased LC3 expression, reduced autophagolysosome numbers, and elevated JNK phosphorylation. Administration of the JNK inhibitor further increased Beclin1 and P62 expression and decreased LC3 expression in the DJ1-silenced cells, whereas opposite effects were observed in the DJ1-overexpressing cells, compared to their respective controls. These findings indicate that DJ1 regulates autophagy in ovarian cancer cells by modulating JNK phosphorylation. DJ1 silencing promoted autophagy, while its overexpression suppressed it. This regulatory mechanism may play a role in ovarian cancer. DJ1 may represent a potential molecular target for therapeutic strategies in ovarian cancer.