Q-omics provides the consensus-scored RPS3 profile across patient tissues and cancer cell-line models. RPS3 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, RPS3 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, RPS3 protein abundance shows 29,212 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, KIRC, and GBM as cancer lineages where RPS3 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 RPS3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RPS3 survival associations across molecular data types. RPS3 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (2) 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 RPS3 RNA expression–survival associations across cancer types. High RPS3 expression shows unfavorable associations in KIRP, ACC, LIHC and HNSC, but favorable associations in UVM and LGG. The KIRP 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 KIRP as the clearest survival context for RPS3 RNA expression.
This table summarizes RPS3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for RPS3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RPS3 shows lower tumor expression in BRCA and higher tumor expression in KIRC, COAD, LIHC, KIRP and LUSC. The KIRC box plot shows higher RPS3 RNA expression in tumor versus normal tissue (log2 FC = +0.865, t-test p < 0.001).
This table shows molecular features associated with RPS3 in patient tissues and cancer cell lines. In patient samples, RPS3 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, RPS3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and CNS.
