Q-omics provides the consensus-scored MCU profile across patient tissues and cancer cell-line models. MCU expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, MCU is differentially expressed in 14, with the highest sampling consensus in KIRP. Additionally, MCU RNA expression shows 20,062 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight MESO, KIRP, and ACC as cancer lineages where MCU 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 MCU — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MCU survival associations across molecular data types. MCU RNA expression shows survival associations in the most cancer types (25), followed by mutation status (1) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MCU RNA expression–survival associations across cancer types. High MCU expression shows unfavorable associations in MESO, ACC, UVM and LIHC, but favorable associations in KIRC and SKCM. 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 MCU RNA expression.
This table summarizes MCU tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRP for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for MCU. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MCU shows lower tumor expression in COAD and higher tumor expression in KIRP, LIHC, LUAD, STAD and THCA. The KIRP box plot shows higher MCU RNA expression in tumor versus normal tissue (log2 FC = +2.270, t-test p < 0.001).
This table shows molecular features associated with MCU in patient tissues and cancer cell lines. In patient samples, MCU 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, MCU RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and BONE.
