Table IV.
Biological process and pathway analysis of genes whose products are negatively correlated with CCNF expression.
| Factor | P-value | Number of genes | Gene list |
|---|---|---|---|
| Biological process | |||
| Regulation of apoptotic process | 1.26E-12 | 19 | GATA3, GATA6, CDKN1B, FOXO3, PRKCA, ERBB2, BCL2, CAV1, MAPK9, BCL2L11, EGFR, PIK3CA, ANXA1, AXL, AR, ARAF, PDCD4, ESR1, TP53 |
| Regulation of intracellular signal transduction | 7.99E-12 | 19 | SHC1, GATA3, PRKCA, ERBB2, BCL2, CAV1, MAPK9, BCL2L11, EGFR, PIK3CA, COPS5, AXL, AR, ARAF, PDCD4, ESR1, INPP4B, TP53, PECAM1 |
| Apoptotic process | 2.63E-11 | 19 | GATA3, GATA6, CDKN1B, FOXO3, PRKCA, ERBB2, BCL2, CAV1, MAPK9, BCL2L11, EGFR, PIK3CA, ANXA1, AXL, AR, ARAF, PDCD4, ESR1, TP53 |
| Negative regulation of apoptotic process | 3.01E-11 | 15 | GATA3, GATA6, CDKN1B, PRKCA, ERBB2, BCL2, CAV1, EGFR, PIK3CA, ANXA1, AXL, AR, ARAF, PDCD4, TP53 |
| Positive regulation of cellular protein metabolic process | 1.08E-10 | 17 | SHC1, GATA3, CDKN1B, PRKCA, ERBB2, BCL2, ITGA2, CAV1, MAPK9, BCL2L11, EGFR, PIK3CA, AR, ARAF, ESR1, TP53, PECAM1 |
| Regulation of protein modification process | 1.30E-10 | 18 | SHC1, GATA3, CDKN1B, PRKCA, ERBB2, BCL2, ITGA2, CAV1, MAPK9, EGFR, PIK3CA, COPS5, AR, ARAF, PDCD4, ESR1, TP53, PECAM1 |
| Positive regulation of signaling | 3.37E-10 | 17 | SHC1, GATA3, GATA6, PRKCA, ERBB2, BCL2, ITGA2, CAV1, MAPK9, BCL2L11, EGFR, AXL, AR, ARAF, ESR1, TP53, PECAM1 |
| Positive regulation of cell communication | 3.61E-10 | 17 | SHC1, GATA3, GATA6, PRKCA, ERBB2, BCL2, ITGA2, CAV1, MAPK9, BCL2L11, EGFR, AXL, AR, ARAF, ESR1, TP53, PECAM1 |
| Regulation of phosphorylation | 7.58E-10 | 16 | SHC1, CDKN1B, PRKCA, ERBB2, BCL2, CAV1, MAPK9, EGFR, PIK3CA, COPS5, AR, ARAF, PDCD4, ESR1, TP53, PECAM1 |
| Positive regulation of phosphorylation | 7.76E-10 | 14 | SHC1, CDKN1B, PRKCA, ERBB2, BCL2, CAV1, MAPK9, EGFR, PIK3CA, AR, ARAF, ESR1, TP53, PECAM1 |
| Regulation of cell proliferation | 2.67E-09 | 16 | SHC1, GATA3, GATA6, CDKN1B, FOXO3, PRKCA, ERBB2, BCL2, RAB25, ITGA2, CAV1, EGFR, ANXA1, AR, ESR1, TP53 |
| Positive regulation of cell proliferation | 4.30E-09 | 13 | SHC1, GATA6, CDKN1B, PRKCA, ERBB2, BCL2, RAB25, ITGA2, CAV1, EGFR, ANXA1, AR, ESR1 |
| Cell adhesion | 1.11E-07 | 14 | SHC1, GATA3, PRKCA, ERBB2, BCL2, ITGA2, CAV1, BCL2L11, EGFR, PIK3CA, ANXA1, AXL, TP53, PECAM1 |
| Positive regulation of apoptotic process | 3.01E-07 | 10 | GATA6, CDKN1B, FOXO3, BCL2, CAV1, MAPK9, BCL2L11, ANXA1, PDCD4, TP53 |
| Pathway | |||
| EGFR tyrosine kinase inhibitor resistance | 2.50E-13 | 10 | SHC1, FOXO3, PRKCA, ERBB2, BCL2, BCL2L11, EGFR, PIK3CA, AXL, ARAF |
| Endocrine resistance | 9.60E-13 | 10 | SHC1, CDKN1B, ERBB2, BCL2, MAPK9, EGFR, PIK3CA, ARAF, ESR1, TP53 |
| Proteoglycans in cancer | 1.01E-09 | 10 | PRKCA, ERBB2, ITGA2, CAV1, EGFR, PIK3CA, ARAF, PDCD4, ESR1, TP53 |
| ErbB signaling pathway | 1.01E-09 | 8 | SHC1, CDKN1B, PRKCA, ERBB2, MAPK9, EGFR, PIK3CA, ARAF |
| Focal adhesion | 1.57E-08 | 9 | SHC1, PRKCA, ERBB2, BCL2, ITGA2, CAV1, MAPK9, EGFR, PIK3CA |
| Pathways in cancer | 1.57E-08 | 11 | CDKN1B, PRKCA, ERBB2, BCL2, ITGA2, MAPK9, EGFR, PIK3CA, AR, ARAF, TP53 |
| MicroRNAs in cancer | 2.01E-08 | 10 | SHC1, CDKN1B, PRKCA, ERBB2, BCL2, BCL2L11, EGFR, PIK3CA, PDCD4, TP53 |
| FoxO signaling pathway | 4.15E-07 | 7 | CDKN1B, FOXO3, MAPK9, BCL2L11, EGFR, PIK3CA, ARAF |
| Signaling by SCF-KIT | 7.61E-07 | 9 | SHC1, CDKN1B, FOXO3, PRKCA, ERBB2, EGFR, PIK3CA, ARAF, TP53 |
| PI3K-Akt signaling pathway | 7.61E-07 | 9 | CDKN1B, FOXO3, PRKCA, BCL2, ITGA2, BCL2L11, EGFR, PIK3CA, TP53 |
| Signaling by NGF | 9.31E-07 | 10 | SHC1, CDKN1B, FOXO3, PRKCA, ERBB2, BCL2L11, EGFR, PIK3CA, ARAF, TP53 |
| HIF-1 signaling pathway | 1.43E-06 | 6 | CDKN1B, PRKCA, ERBB2, BCL2, EGFR, PIK3CA |
| Apoptosis signaling pathway | 1.43E-06 | 6 | PRKCA, BCL2, MAPK9, BCL2L11, PIK3CA, TP53 |
| Signaling by ERBB2 | 1.54E-06 | 5 | SHC1, PRKCA, ERBB2, EGFR, PIK3CA |
CCNF, cyclin F; SCF, Skp, Cullin, F-box containing. P-values were corrected for multiple comparisons using the false discovery rate (FDR) (Benjamini and Hochberg).