Overexpression of TRIM44 mediates the NF-κB pathway to promote the progression of ovarian cancer

BackgroundOvarian cancer (OC) is the second most commonly seen cancer in the US, and patients with OC are commonly diagnosed in the advanced stage. Research into the molecular mechanisms and potential therapeutic targets of OC is becoming increasingly urgent. In our study, we worked to discover the role of TRIM44 in OC development.ObjectiveThis study explored whether the overexpression of TRIM44 mediates the NF-kB pathway to promote the progression of OC.MethodsA TRIM44 overexpression model was constructed in SKOV3 cells, and the proliferation ability of the cells was detected using the CCK-8 assay. The migration healing ability of cells was detected using cell scratch assay. Cell migration and invasion were detected using Transwell nesting. TUNEL was applied to detect apoptosis, and ELISA and western blot were used to detect the expression of NF-kappa B signaling pathway proteins. The pathological changes of the tumor tissues were observed using HE staining in a mouse ovarian cancer xenograft model. Immunofluorescence double staining, RT-PCR, and western blot were used to determine the expression of relevant factors in tumour tissues.ResultsTRIM44 overexpression promoted the proliferation, migration, and invasion of SKOV3 cells in vitro and inhibited apoptosis while enhancing the growth of tumours in vivo. TRIM44 regulated the NF-kappa B signaling pathway.ConclusionsTRIM44 overexpression can regulate the NF-kappa B signaling pathway to promote the progression of OC, and TRIM44 may be a potential therapeutic target for OC.