Conclusion
Hence, TRIM11 regulates CC cell progression by modulating PI3K/AKT pathway. The results suggested that TRIM11 might be a possible target for the diagnosis and prognosis of CC patients.
Methods
First, the expression pattern and function of TRIM11 in CC were inferred by GEPIA database. The expression of TRIM11 in CC tissues and cells was verified by RT-qPCR and Western blot assays. TRIM11 shRNA was transfected into CC cells. The effect of TRIM11 knockdown on CC cell proliferation and cell apoptosis was assessed by CCK-8 assay, clone formation test and flow cytometry (FCM). Furthermore, the effect of TRIM11 knockdown on cell migration and invasion was measured by Transwell assay. The apoptosis-related proteins (Bax, Bcl-2 and Cleaved caspase 3) and PI3K/AKT pathway-related proteins (PI3K, p-PI3K, AKT and p-Akt) were examined by Western blot assay.
Objective
To detect the expression pattern of TRIM11 in CC and to investigate the effect of TRIM11 knockdown on CC progression.
Results
TRIM11 was found to be dramatically upregulated in CC tissues and cells. Besides this, TRIM11 was closely related to FIGO stage, infiltration depth and metastasis. Moreover, high expression of TRIM11 was found to be associated with poor prognosis of CC patients. Functional experiments showed that knockdown of TRIM11 obviously suppressed CC cell proliferation, migration and invasion, while accelerated cell apoptosis. In addition, the PI3K inhibitor (LY294002) was used to assess the connection between PI3K/AKT pathway and TRIM11 in CC cells. We found that TRIM11 overexpression suppressed the phosphorylation of PI3K and AKT in CC cells.