Overexpression of TRIM44 mediates the NF-kB pathway to promote OC progression and metastasis

Background: TRIM44 is highly expressed in both ovarian cancer tissues and cells, and is significantly associated with clinicopathological factors and poor prognosis. However, its effect on the malignant biological behavior of ovarian cancer cells and its potential mechanism of action have not been revealed. Therefore, we aimed to investigate the role and potential mechanism of TRIM44 on ovarian cancer. Methods: : Using shRNA transfection to overexpress TRIM44, we investigated the effects of TRIM44 overexpression on the proliferation, migration, invasion and apoptosis of ovarian cancer cells and the growth ability of xenograft tumors through in vivo xenograft mouse models and in vitro experiments. In addition, to further elucidate its molecular mechanisms of action affecting ovarian cancer progression and metastasis. Results: : TRIM44 overexpression significantly promoted the proliferation, migration, and invasion of SKOV3 cells and inhibited apoptosis in vitro while promoting tumor growth in vivo. Mechanistic studies have shown that TRIM44 overexpression contributes to ovarian cancer cells invasion, metastasis, and anti-apoptosis by upregulating the levels of inflammatory cytokines (TNF-α, IL-1β, IL-8) in the tumor microenvironment, stimulating the secretion of IKKβ factors, further promoting IKBα degradation and phosphorylation, initiating NF-kB p65 entry into the nucleus, and activating the NF-kB signaling pathway to upregulate or downregulate the expression of Metallo-matrix protease (MMP-9), and apoptotic genes (Bcl-2, Caspase-3). Conclusions: : These data suggest that TRIM44 overexpression promotes ovarian cancer progression and metastasis by promoting NF-kB signaling pathway activation. These results provide evidence for TRIM44 as an oncogene in ovarian cancer and suggest that it may be a potential target for ovarian cancer therapy.