Q-omics provides the consensus-scored MMP25 profile across patient tissues and cancer cell-line models. MMP25 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, MMP25 is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, MMP25 RNA expression shows 14,374 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight HNSC, KIRC, and TGCT as cancer lineages where MMP25 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 MMP25 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MMP25 survival associations across molecular data types. MMP25 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (8) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MMP25 RNA expression–survival associations across cancer types. High MMP25 expression shows unfavorable associations in UVM, LUSC and LGG, but favorable associations in HNSC, SKCM and BRCA. The HNSC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify HNSC as the clearest survival context for MMP25 RNA expression.
This table summarizes MMP25 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for MMP25. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MMP25 shows lower tumor expression in COAD, LUSC and LUAD and higher tumor expression in KIRC, STAD and ESCA. The KIRC box plot shows higher MMP25 RNA expression in tumor versus normal tissue (log2 FC = +0.812, t-test p < 0.001).
This table shows molecular features associated with MMP25 in patient tissues and cancer cell lines. In patient samples, MMP25 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, MMP25 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 CNS and LARGE_INTESTINE.
