E3 ubiquitin ligase F-box only
protein 22 (FBXO22), which targets the key regulators of cellular activities for ubiquitylation and degradation, plays an important role in
tumorigenesis and
metastasis. However, the function of FBXO22 in
epithelial ovarian cancers has not been reported. This study aims to explore the
biological function of FBXO22 in
epithelial ovarian cancers progression and
metastasis and its specific regulation mechanism. Immunohistochemistry analysis of tissue microarray was performed to evaluate the expression of FBXO22 in
epithelial ovarian cancers patients. The proliferative ability of
epithelial ovarian cancers cells was examined by the CCK8. The
metastasis ability was detected by the wound healing assay, migration and invasion assays. Western blot was used to verify the relationship between FBXO22 expression and
mitogen-activated protein kinase related
proteins. Autophagic flux was detected by electron microscopy, mRFP-GFP-LC3 adenovirus, lysosomal tracker and western blot. For in vivo experiments, the effect of FBXO22 on
epithelial ovarian cancers resistance was observed in a xenograft
tumor model and a metastatic mice model. We found that FBXO22 expression was significantly increased in
epithelial ovarian cancers tissues and was closely correlated with clinical pathological factors. As a result, we found that FBXO22 promoted the growth and
metastasis, as well as inhibited the autophagy flux. In addition, we identified that FBXO22 performed these functions via the MAPK/ERK pathway. Our results first reported the function of FBXO22 in
epithelial ovarian cancer and the correlation between FBXO22 and autophagy, suggesting FBXO22 as a novel target of
epithelial ovarian cancers assessment and treatment.