solute carrier family 52 member 3Genealiases: BVVLS · BVVLS1 · C20orf54 · RFT2 · RFVT3 · bA371L19.1
Q-omics provides the consensus-scored SLC52A3 profile across patient tissues and cancer cell-line models. SLC52A3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in STAD. Among the 18 cancer types available for tumor–normal comparison, SLC52A3 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, SLC52A3 protein abundance shows 15,400 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight STAD, KIRC, and LUAD as cancer lineages where SLC52A3 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 SLC52A3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SLC52A3 survival associations across molecular data types. SLC52A3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) 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 SLC52A3 RNA expression–survival associations across cancer types. High SLC52A3 expression shows unfavorable associations in KIRP, PAAD, ESCA and LUAD, but favorable associations in STAD and SARC. The STAD 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 STAD as the clearest survival context for SLC52A3 RNA expression.
This table summarizes SLC52A3 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 3. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for SLC52A3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SLC52A3 shows lower tumor expression in KIRC and KIRP and higher tumor expression in THCA, LUAD, LIHC and LUSC. The KIRC box plot shows higher SLC52A3 RNA expression in normal versus tumor tissue (log2 FC = −2.976, t-test p < 0.001).
This table shows molecular features associated with SLC52A3 in patient tissues and cancer cell lines. In patient samples, SLC52A3 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, SLC52A3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and STOMACH.
