Q-omics provides the consensus-scored SMCO3 profile across patient tissues and cancer cell-line models. SMCO3 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, SMCO3 is differentially expressed in 9, with the highest sampling consensus in THCA. Additionally, SMCO3 protein abundance shows 15,434 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, THCA, and LSCC as cancer lineages where SMCO3 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 SMCO3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SMCO3 survival associations across molecular data types. SMCO3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) 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 SMCO3 RNA expression–survival associations across cancer types. High SMCO3 expression shows unfavorable associations in KIRC, COAD, KIRP and LGG, but favorable associations in UVM and OV. 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 SMCO3 RNA expression.
This table summarizes SMCO3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 3. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for SMCO3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SMCO3 shows lower tumor expression in THCA, KICH, LUAD, KIRC, KIRP and LUSC. The THCA box plot shows higher SMCO3 RNA expression in normal versus tumor tissue (log2 FC = −2.132, t-test p < 0.001).
This table shows molecular features associated with SMCO3 in patient tissues and cancer cell lines. In patient samples, SMCO3 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, SMCO3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Leukemia.
