Q-omics provides the consensus-scored MMP3 profile across patient tissues and cancer cell-line models. MMP3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, MMP3 is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, MMP3 RNA expression shows 14,430 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, HNSC, and LSCC as cancer lineages where MMP3 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 MMP3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MMP3 survival associations across molecular data types. MMP3 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 MMP3 RNA expression–survival associations across cancer types. High MMP3 expression shows unfavorable associations in UVM, KIRC, ACC and KICH, but favorable associations in UCEC and COAD. The UVM 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 UVM as the clearest survival context for MMP3 RNA expression.
This table summarizes MMP3 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 HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for MMP3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MMP3 shows higher tumor expression in HNSC, COAD, LUAD, STAD, READ and LUSC. The HNSC box plot shows higher MMP3 RNA expression in tumor versus normal tissue (log2 FC = +6.421, t-test p < 0.001).
This table shows molecular features associated with MMP3 in patient tissues and cancer cell lines. In patient samples, MMP3 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, MMP3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and LARGE_INTESTINE.
