Research Paper Volume 13, Issue 2 pp 2803—2821

SPC25 overexpression promotes tumor proliferation and is prognostic of poor survival in hepatocellular carcinoma

Mechanistic investigation into how SPC25 promotes HCCs growth. (A) Gene Set Enrichment Analysis (GSEA) shows statistically significant different biological function between subgroups of high SPC25 level and low SPC25 level. (B) STRING analysis of interactions between SPC25 and other proteins. (C) Correlation between SPC25 and cell cycle-regulation related genes, including CDK1, cdc25A, Cyclin A2, Cyclin B1, Cyclin D1, Cyclin E1. (D) Two siRNAs (si#1 and si#2) against SPC25 effectively silenced SPC25 expression, as determined by qRT-PCR. Negative control siRNA (siNC) and β-actin were used as negative and endogenous controls, respectively. The data are represented as the mean ± s.d. of three independent experiments. **P E) Silencing SPC25 decreased the protein level of SPC25, CDK1, cdc25A, Cyclin A2, Cyclin B1, Cyclin D1, and Cyclin E1.

Figure 7. Mechanistic investigation into how SPC25 promotes HCCs growth. (A) Gene Set Enrichment Analysis (GSEA) shows statistically significant different biological function between subgroups of high SPC25 level and low SPC25 level. (B) STRING analysis of interactions between SPC25 and other proteins. (C) Correlation between SPC25 and cell cycle-regulation related genes, including CDK1, cdc25A, Cyclin A2, Cyclin B1, Cyclin D1, Cyclin E1. (D) Two siRNAs (si#1 and si#2) against SPC25 effectively silenced SPC25 expression, as determined by qRT-PCR. Negative control siRNA (siNC) and β-actin were used as negative and endogenous controls, respectively. The data are represented as the mean ± s.d. of three independent experiments. **P < 0.01. (E) Silencing SPC25 decreased the protein level of SPC25, CDK1, cdc25A, Cyclin A2, Cyclin B1, Cyclin D1, and Cyclin E1.