Background: Lung adenocarcinoma (LUAD) has high morbidity and mortality. Current studies indicate nucleoporin 107 (NUP107) is involved in the construction of nuclear pore complex, and NUP107 overexpression contributes to the growth and development in most types of cancers, but its effect in LUAD has not been elucidated. Methods: Differences in NUP107 expression were investigated using the Cancer Genome Atlas (TCGA) and multiple Gene Expression Omnibus (GEO) data sets. Enrichment analysis were implemented to probe the NUP107 function. The association of NUP107 with the degree of immune cell infiltration was investigated by the TIMER database, single-sample gene set enrichment analysis (ssGSEA), and ESTIMATE. The association of NUP107 expression with tumor mutation burden (TMB), TP53, and immune checkpoint was analyzed. Single-cell RNA sequencing data were used to detect NUP107 expression in different cell clusters. Finally, we performed real-time quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC) to prove the difference of NUP107 expression. Results: NUP107 was overexpressed in LUAD and mainly expressed in cancer stem cell (CSC). Overexpression of NUP107 in LUAD suggested a poorer prognosis. Functional enrichment analysis pointed out that NUP107 was mainly linked to the regulation of cell cycle. Both immune cell infiltration and TMB were found to be in connection with NUP107. Cases in the group with high NUP107 expression had poorer immune infiltration, but had higher expression of immune checkpoints, TMB, and proportion of TP53 mutations. Conclusion: NUP107 is a sensitive diagnostic and prognostic factor for LUAD and may be involved in tumor progression through its effects on cell cycle and immune infiltration.

The most common type of non-small cell lung cancer is lung adenocarcinoma (LUAD), which is characterized by high morbidity and poor survival. Up-regulation of SASS6 expression can lead to the progression of various malignant tumors. However, there are no relevant studies on the role of SASS6 in LUAD. SASS6 was highly expressed in most tumors, reflecting a good diagnostic value, and its overexpression in LUAD indicated discouraging overall prognosis. Functional enrichment analysis suggested that SASS6 was associated with cell cycle in LUAD. In addition, patients with high SASS6 expression had worse immune infiltration, but higher TMB and immune checkpoint, and higher sensitivity to multiple targeted drugs such as osimertinib. Cell experiments confirmed that knockdown of SASS6 could inhibit the viability of tumor cells.SASS6 has important value in the diagnosis of cancer. In particular, SASS6 is a crucial factor in the progression of LUAD, and has important clinical value, especially in the diagnosis, prognosis and treatment

Background: Phosducin-like 3 (PDCL3), a member of the photoreceptor family, is involved in angiogenesis and apoptosis. However, there is no pan-cancer analysis, and few studies have explored the effect of PDCL3 on tumor immune infiltration.Method: Public datasets were used to explore the diagnostic and prognostic value of PDCL3. The relationship between PDCL3 expression and immune infiltration, tumor mutation burden (TMB), and microsatellite instability (MSI) was investigated. Additionally, the therapeutic value of PDCL3 was explored. Finally, differences in PDCL3 expression across cell clusters were analyzed using single-cell datasets. In vitro cellular assays were performed to assess the impact of PDCL3 expression on the proliferative capacity, migratory potential, and invasive properties of non-small cell lung cancer (NSCLC) cells.Results: PDCL3 expression was upregulated in most tumors and correlated with poor outcomes, showing diagnostic and prognostic value. In addition, PDCL3 expression exhibited a positive correlation with infiltration of T helper 2 (Th2) cells and a negative correlation with infiltration of plasmacytoid dendritic cells (pDCs) across a variety of tumors. A relationship was also found between PDCL3 expression and TMB and MSI. Single-cell dataset analysis confirmed that PDCL3 expression was primarily in cancer cells and macrophages. In vitro functional analyses demonstrated that genetic silencing of PDCL3 significantly reduced proliferative rates, migratory activity, and invasive potential in pulmonary carcinoma cell models.Conclusions: PDCL3 may contribute to cancer progression and is a potential candidate biomarker for pan-cancer diagnosis and prognosis. These findings suggest that targeting PDCL3 may provide a valuable strategy for cancer immunotherapy.