Background: Upregulation of the six-transmembrane epithelial antigen of prostate-1 (STEAP1) is closely associated with prognosis of numerous malignant cancers. However, its role in lung adenocarcinoma (LUAD), the most common type of lung cancer, remains unknown. This study aimed to investigate the role of STEAP1 in the occurrence and progression of LUAD and the potential mechanisms underlying its regulatory effects. Methods: STEAP1 mRNA and protein expression were analyzed in 40 LUAD patients via real-time PCR and western blotting, respectively. We accessed the clinical data of 522 LUAD patients from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) to investigate the expression and prognostic role of STEAP1 in LUAD. Further, we performed gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and gene set enrichment analysis (GSEA) to elucidate the potential mechanism underlying the role of STEAP1 in LUAD. The protein-protein interaction (PPI) network of STEAP1 was analyzed using the Search Tool for the Retrieval of Interacting Genes (STRING) database, and hub genes with significant positive and negative associations with STEAP1 were identified and their role in LUAD prognosis was predicted. Results: STEAP1 was significantly upregulated in LUAD patients and associated with LUAD prognosis. Further, TCGA data indicated that STEAP1 upregulation is correlated with the clinical prognosis of LUAD. GO and KEGG analysis revealed that the genes co-expressed with STEAP1 were primarily involved in cell division, DNA replication, cell cycle, apoptosis, cytokine signaling, NF-kB signaling, and TNF signaling. GSEA revealed that homologous recombination, p53 signaling pathway, cell cycle, DNA replication, apoptosis, and toll-like receptor signaling were highly enriched upon STEAP1 upregulation. Gene Expression Profiling Interactive Analysis (GEPIA) analysis revealed that the top 10 hub genes associated with STEAP1 expression were also associated with the LUAD prognosis. Conclusion: STEAP1 upregulation potentially influences the occurrence and progression of LUAD and its co-expressed genes via regulation of homologous recombination, p53 signaling, cell cycle, DNA replication, and apoptosis. STEAP1 is a potential prognostic biomarker for LUAD.

Background: The expression of progestin and adipoQ receptor 3 (PAQR3) is generally downregulated in multiple tumors, which is associated with tumor progression and poor prognosis. Methods: The clinical value of PAQR3 was analyzed using various databases and in 60 patients with non-small cell lung cancer (NSCLC). In addition, cell counting kit-8 (CCK-8), colony formation, and flow cytometry assays were used to evaluate the effect of PAQR3 on the growth of NSCLC cells in vitro. Gene set enrichment analysis (GSEA) was performed to investigate the possible mechanism through which PAQR3 is involved in the progression of lung cancer. Furthermore, western blotting was employed to verify the relevant mechanism. Results: The expression of PAQR3 was decreased in 60 NSCLC patients and was related to the histological subtype, lymph node metastasis, tumor size, and diagnosis of NSCLC. Patients with lung adenocarcinoma with increased PAQR3 expression tended to have a better prognosis. Besides, PAQR3 inhibited proliferation, clone formation, and cycle transition in NSCLC cells, but induced apoptosis. The results of GSEA showed that PAQR3 regulated the progression of lung cancer by affecting cell cycle, DNA replication, and the p53 signaling pathway. We confirmed that PAQR3 overexpression inhibited the expression of NF-κB, while it increased the expression of p53, phosph-p53, and Bax. On the contrary, PAQR3 inhibition played an opposite role in these proteins. Conclusions: PAQR3 inhibited the growth of NSCLC cells through the NF-κB/P53/Bax signaling pathway and might be a new target for diagnosis and treatment.

Nuclear factor (erythroid-derived 2)-like (Nrf)2 and metallothionein have been implicated in carcinogenesis. This study investigated the expression of Nrf2 and of Nrf2-targeted genes (NQO1 and GCLC) and the genes for the metallothionein (MT) isoforms (MT-1A and MT-2A) in human lung cancer and cancer-surrounding tissues.

Post‑translational modifications (PTMs) of proteins influence their functionality by altering the structure of precursor proteins. These modifications are closely linked to tumor progression through the regulation of processes such as cell proliferation, apoptosis, angiogenesis and invasion. Tumors produce large amounts of lactic acid through aerobic glycolysis. Lactic acid not only serves an important role in cell metabolism, but also serves an important role in cell communication. Lactylation, a PTM involving lactate and lysine residues as substrates, serves as an epigenetic regulator that modulates intracellular signaling, gene expression and protein function, thereby serving a crucial role in tumorigenesis and progression. The identification of lactylation provides a key breakthrough in elucidating the interaction between tumor metabolic reprogramming and epigenetic modification. The present review primarily summarizes the occurrence of lactylation, its effect on tumor progression, drug resistance, the tumor microenvironment and gut microbiota, and its potential as a therapeutic target for cancer. The aim of the present review was to provide novel strategies for potential cancer therapies.

Purpose: The clinical outcomes of delayed chest closure (DCC) compared with primary chest closure (PCC) following lung transplantation, including perioperative outcomes and long-term survival, remained controversial. This was the first systematic review and meta-analysis aimed to identify the short- and long-term outcomes of DCC following lung transplantation. Methods: We comprehensively searched electronic literature from 4 databases up to April 1st, 2022. Dichotomous data and continuous data were pooled with odds ratio and weighted mean difference, respectively. The quality of included studies was assessed with the Newcastle–Ottawa Scale. Results: Ten studies were included in the systematic review and 4 studies were included in the meta-analysis. Pooled analysis showed that DCC was associated with an increased risk of surgical site infection, prolonged hospital stays, and higher risk of primary graft dysfunction compared to PCC. The 30 day and 5 year survival were higher in PCC cohort compared with DCC cohort while differences in survival at 6 months was insignificant. Conclusion: Our findings do not support the aggressive application of DCC. DCC should be cautiously applied since its association with worse perioperative outcomes and higher mortality. But it remains the life-saving steps under dangerous circumstances.

This study aimed to investigate the potential association between white blood cell counts and the risk of lung cancer, including its subtypes, through Mendelian randomization (MR) analysis. We conducted a two-sample MR analysis using genome-wide association study (GWAS) summary statistics for the both exposure traits (eosinophil count, neutrophil count, lymphocyte count, monocyte count, basophil count, and total white blood cell count) and outcome traits (lung cancer and its subtypes). The GWAS dataset for lung cancer included 29,266 cases (11273 lung adenocarcinoma (LUAD), 7426 lung squamous cell carcinoma (LSCC), 2664 small cell lung cancer (SCLC)) and 56,450 controls. In MR analysis, we employed methods such as Inverse variance weighted (IVW), weighted median, MR-Egger regression, MR pleiotropy residual sum and outlier. MR analysis revealed an elevated total white blood cell (WBC) count significantly increased the risk of LUAD (IVW: OR = 1.484, 95% CI = 1.219–1.749, p = 0.003). The results confirmed a causal relationship between monocyte count and LUAD (IVW: OR = 1.687, 95% CI:1.542–1.830, p < 0.001). An increased total WBC count was associated with a higher risk of LUAD. Additionally, analysis of WBC subtypes counts indicated that monocyte count plays an crucial role in the elevated risk of LUAD.