Q-omics provides the consensus-scored PLIN3 profile across patient tissues and cancer cell-line models. PLIN3 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PLIN3 is differentially expressed in 9, with the highest sampling consensus in KIRP. Additionally, PLIN3 protein abundance shows 30,565 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight UVM, KIRP, and HNSC as cancer lineages where PLIN3 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 PLIN3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PLIN3 survival associations across molecular data types. PLIN3 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (5) 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 PLIN3 RNA expression–survival associations across cancer types. High PLIN3 expression shows unfavorable associations in UVM, MESO, LUAD and LIHC, but favorable associations in SCLC and UCEC. 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 PLIN3 RNA expression.
This table summarizes PLIN3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PLIN3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PLIN3 shows higher tumor expression in KIRP, KIRC, LUAD, LIHC, LUSC and BLCA. The KIRP box plot shows higher PLIN3 RNA expression in tumor versus normal tissue (log2 FC = +1.047, t-test p < 0.001).
This table shows molecular features associated with PLIN3 in patient tissues and cancer cell lines. In patient samples, PLIN3 shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, PLIN3 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 SKIN and BONE.
