Chaperonin containing TCP-1 subunit 7 as a prognostic biomarker linking immune infiltration and PI3K/AKT signaling in lung adenocarcinoma

Lung adenocarcinoma (LUAD) is the most common non-small cell lung cancer, with high incidence and poor prognosis. Disruption of cytoskeletal protein folding by the chaperonin containing TCP-1 (CCT) can drive tumor progression. However, the role of chaperonin containing TCP-1 subunit 7 (CCT7) in LUAD remains largely unstudied. We conducted a multi-database characterization of CCT7 in LUAD, covering its diagnostic and prognostic value, upstream miRNAs, drug sensitivity, gene mutations, immune characteristics, and pathway enrichment. Single-cell data were then used to profile CCT7 expression heterogeneity across cell clusters and over time. In vitro experiments validated the impact of CCT7 knockdown on cancer cells, with Western blotting confirming modulation of the PI3K/AKT pathway. CCT7 is abnormally overexpressed in LUAD, particularly in advanced stages, and its elevated expression predicts a poor prognosis. Moreover, CCT7 levels correlate significantly with tumor mutation burden (TMB) and immune infiltration. Single-cell data revealed that CCT7 is expressed across multiple immune cell types, and pseudotime analysis revealed a progressive increase in CCT7 expression along the inferred trajectory from monocytes to lipid-associated macrophages (LAMs). Functional enrichment analysis of differentially expressed genes between these two cell types identified the PI3K/AKT pathway, and this pathway was also enriched among CCT7-associated genes. In our cell experiments, knockdown of CCT7 impaired the proliferation, wound closure, and invasion of lung cancer cells. Western blotting further confirmed that CCT7 silencing reduced the phosphorylation levels of PI3K and AKT. CCT7 may represent a candidate biomarker with potential diagnostic and prognostic value in LUAD. Its expression is associated with an immunosuppressive microenvironment and pro-tumorigenic phenotypes, and may be linked to the PI3K/AKT signaling axis.