Abstract
The role of Sun2 has been described by previous studies in various types of cancers, including breast cancer and lung cancer. However, its role and potential molecular mechanism in the progression of prostate cancer have not been fully elucidated. In the present study, we found that Sun2 expression was reduced in prostate cancer tissues compared with paired normal tissues, and that low expression of Sun2 was significantly correlated with Higher Gleason scores, postoperative T stage (pT), Lymph nodal invasion and Clinical pathological stages. In addition, reduced Sun2 Expression predicts poor survival of prostate cancer patients and could serve as an independent predictor of prostate cancer patients overall survival (OS).Furthermore, Sun2 overexpression inhibits the prostate cancer cells growth, and Sun2 knockdown promotes the prostate cancer cells growth both in vitro and vivo. Mechanical silencing of , Sun2 promoted fatty acid oxidation (FAO) in prostate cancer, prostate cancer cells growth promoted by Sun2 silencing could be reversed by the FAO inhibitor Etomoxir. Additionally, we also showed that serum amyloid A1 (SAA1) play a vital role in FAO, ATP and cell growth promoted by Sun2 loss in prostate cancer. These results suggest that Loss of Sun2 promoted the prostate cancer progression by regulating FAO.