transmembrane protein 176AGenealiases: GS188 · HCA112 · MS4B1
Q-omics provides the consensus-scored TMEM176A profile across patient tissues and cancer cell-line models. TMEM176A expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, TMEM176A is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, TMEM176A RNA expression shows 19,112 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, KIRC, and LSCC as cancer lineages where TMEM176A 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 TMEM176A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TMEM176A survival associations across molecular data types. TMEM176A RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TMEM176A RNA expression–survival associations across cancer types. High TMEM176A expression shows unfavorable associations in LGG and LUSC, but favorable associations in SKCM, KIRC, HNSC and SCLC. The SKCM 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 SKCM as the clearest survival context for TMEM176A RNA expression.
This table summarizes TMEM176A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TMEM176A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TMEM176A shows lower tumor expression in KICH and BRCA and higher tumor expression in KIRC, STAD, THCA and LUAD. The KIRC box plot shows higher TMEM176A RNA expression in tumor versus normal tissue (log2 FC = +1.707, t-test p < 0.001).
This table shows molecular features associated with TMEM176A in patient tissues and cancer cell lines. In patient samples, TMEM176A 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, TMEM176A 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 BREAST and LARGE_INTESTINE.
