cleavage and polyadenylation specific factor 3Genealiases: CPSF-73 · CPSF73 · NEDMHS · NEDMHSN
Q-omics provides the consensus-scored CPSF3 profile across patient tissues and cancer cell-line models. CPSF3 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, CPSF3 is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, CPSF3 protein abundance shows 32,610 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where CPSF3 shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for CPSF3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CPSF3 survival associations across molecular data types. CPSF3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CPSF3 RNA expression–survival associations across cancer types. High CPSF3 expression shows unfavorable associations in MESO, KIRP, ACC, LIHC and BLCA, but favorable associations in LUSC. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify MESO as the clearest survival context for CPSF3 RNA expression.
This table summarizes CPSF3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CPSF3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CPSF3 shows higher tumor expression in HNSC, COAD, LUAD, BLCA, LIHC and LUSC. The HNSC box plot shows higher CPSF3 RNA expression in tumor versus normal tissue (log2 FC = +1.077, t-test p < 0.001).
This table shows molecular features associated with CPSF3 in patient tissues and cancer cell lines. In patient samples, CPSF3 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, CPSF3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in LIVER and UPPER_AERODIGESTIVE_TRACT.
