Q-omics provides the consensus-scored PKP3 profile across patient tissues and cancer cell-line models. PKP3 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PKP3 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, PKP3 protein abundance shows 21,469 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight KIRC, and HNSC as cancer lineages where PKP3 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 PKP3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PKP3 survival associations across molecular data types. PKP3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PKP3 RNA expression–survival associations across cancer types. High PKP3 expression shows unfavorable associations in KIRC, MESO, LUAD, PAAD, ACC and LUSC. The KIRC 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 KIRC as the clearest survival context for PKP3 RNA expression.
This table summarizes PKP3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for PKP3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PKP3 shows lower tumor expression in KIRC and higher tumor expression in COAD, LUAD, BLCA, LUSC and BRCA. The KIRC box plot shows higher PKP3 RNA expression in normal versus tumor tissue (log2 FC = −1.797, t-test p < 0.001).
This table shows molecular features associated with PKP3 in patient tissues and cancer cell lines. In patient samples, PKP3 shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, PKP3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BONE.
