Q-omics provides the consensus-scored PKN3 profile across patient tissues and cancer cell-line models. PKN3 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, PKN3 is differentially expressed in 15, with the highest sampling consensus in KICH. Additionally, PKN3 RNA expression shows 18,375 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight MESO, KICH, and ACC as cancer lineages where PKN3 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 PKN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PKN3 survival associations across molecular data types. PKN3 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (9) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PKN3 RNA expression–survival associations across cancer types. High PKN3 expression shows unfavorable associations in MESO, ACC, UVM, SKCM and LGG, but favorable associations in KIRC. 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 PKN3 RNA expression.
This table summarizes PKN3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 2. The strongest signals are observed in KICH for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for PKN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PKN3 shows lower tumor expression in KICH and BRCA and higher tumor expression in LIHC, COAD, HNSC and STAD. The KICH box plot shows higher PKN3 RNA expression in normal versus tumor tissue (log2 FC = −1.859, t-test p < 0.001).
This table shows molecular features associated with PKN3 in patient tissues and cancer cell lines. In patient samples, PKN3 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, PKN3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
