Background: Nowadays, controlling nutritional status (CONUT) has been used as a prognostic factor in variety of cancers. However, no consensus has been reached on the prognostic value of CONUT in lung cancer. In this study, we aim to investigate the role of CONUT in survival of patients with lung cancer.Methods: EMBASE, web of science, and Medline were used to search articles in English-language journals.The association between CONUT score and survival of patients with lung cancer was evaluated by using pooled HRs and their 95% CIs. Chi-square test and I-Square was used to test heterogeneity among studies.Analyses were all performed using Stata 13.0 (Stata Corporation, College Station, TX).Results: Eight studies with 1,836 patients were eventually included in this meta-analysis. The pooled results showed that high CONUT score had an unfavorable impact on OS (HR =1.63, 95% CI: 1.30-2.04),

Background: This study aimed to use bioinformatics analysis to compare data from tissue microarrays from patients with lung adenocarcinoma (LUAD) and normal lung tissue, and human lung adenocarcinoma cells with normal lung epithelial cells in vitro to investigate the role of synaptotagmin 12 (SYT12) gene expression in LUAD. Material/Methods: Human lung adenocarcinoma cell lines (A549, SPC-A-1, H1299, H1975, and PC9) and the normal HBE cell line were compared, and tumor xenografts were developed in mice. The Cancer Genome Atlas (TCGA) tissue microarray data were used to compare SYT12 expression and overall survival (OS). The in vivo and in vitro effects of down-regulation and upregulation of SYT12 were studied using short-interfering RNA (si-RNA) and overexpression plasmids, respectively. The Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) pathway analysis, quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and Western blot investigated the molecular mechanisms of SYT12 expression in LUAD. Results: SYT12 expression was increased in tissues from patients with LUAD from TCGA and was associated with advanced tumor stage and reduced prognosis. Knockdown of SYT12 suppressed the proliferation and migration of LUAD cells, and upregulation of SYT12 increased the proliferation and migration of LUAD cells in vitro. Phosphorylation of PIK3R3 activated the PI3K/AKT/mTOR pathway. In the mouse xenograft model, expression of SYT12 increased the volume and weight of the xenograft tumors. Conclusions: Bioinformatics analysis, human LUAD cells, and mouse xenograft studies showed that SYT12 acted as a possible oncogene by phosphorylation of PIK3R3 to activate the PI3K/AKT/mTOR signaling pathway.

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