Fig 1: Network and function of TRIM8 and its substrate genes. (A) Network view of predicted E3-substrate interactions in UbiBrowser web services. In network view, the central node is TRIM8, and the surrounding nodes are the predicted substrates. (B–E) Correlation analysis of TRIM8 and four predictive substrates in cervical cancer. (F) Schematic diagram of interaction of co-expressed miRNA network of TRIM8 and RELA.
Fig 2: TRIM8 plays a role as an oncogene in cervical cancer. (A) Verification of interference efficiency of TRIM8 in SiHa and HeLa cells, respectively. The bottom figures are the corresponding quantization diagrams. (B, C) CCK-8 and clone formation assays showed that down regulation of TRIM8 expression inhibited the proliferation of SiHa and HeLa cells. (D) Flow cytometry indicated that the silence of TRIM8 increased the apoptosis ratio of SiHa cells and HeLa cells. **p < 0.01, ***p < 0.001.
Fig 3: Expression and prognosis of TRIM8 in cervical cancer. (A) The IHC showed that TRIM8 protein is highly expressed in tumor tissues. (B) Statistical results of IHC score of TRIM8. *p < 0.05. (C) Distribution of TRIM8 in cervical cancer cells. (D) Kaplan Meier curve analysis of patients with high and low expression levels of TRIM8.
Fig 4: Identification and analysis of TRIM8. (A) The Venn diagram of 44 ubiquitination-related genes and autophagy -related genes. (B) The ROC curve of TCGA-CESC according to the expression of TRIM8. (C) Distribution of CSCs scores in different groups. G1 represents the low expression group of TRIM8, and G2 the high expression group of TRIM8. ****p < 0.001. (D) The top 15 mutation genes in high and low TRIM8 expression group, respectively.
Fig 5: Analysis of potential drug sensitivity of TRIM8. (A) The Gene Set Cancer Analysis (GSCA). (B) Structure of potential targeted drugs, including trametinib, midostaurin, and dasatinib.
Supplier Page from Abcam for Anti-TRIM8 antibody