Background Lung adenocarcinoma (LUAD) accounts for approximately 40% of all lung cancer patients. There is an urgent need to understand the mechanisms of cancer progression in LUAD and to identify useful biomarkers to predict prognosis. Methods In this study, Oncomine database was used to identify potential genes contributed to cancer progression. Bioinformatics analysis including pathway enrichment and text mining was used to explain the potential roles of identified genes in LUAD. The Cancer Genome Atlas database was used to analyze the association of gene expression with survival result. Results Our results indicated that 80 genes were significantly dysregulated in LUAD according to four microarrays covering 356 cases of LUAD and 164 cases of normal lung tissues. Twenty genes were consistently and stably dysregulated by more than twofold. Ten of 20 genes had a relationship with overall survival or disease‐free survival in a cohort of 516 LUAD patients, and 19 genes were associated with tumor stage, gender, age, lymph node, or smoking. Low expression of AGER and high expression of CCNB1 were specifically associated with poor survival. Conclusion Our findings implicate AGER and CCNB1 might be potential biomarkers for diagnosis and prognosis targets for LUAD.

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In this study, a water-soluble longan seed polysaccharide (WLSP), with a molecular weight of 57 kDa, was isolated from longan seed. Gas chromatography (GC) analysis showed that WLSP was composed mainly of rhamnose (Rha), mannose (Man), arabinose (Ara), galactose (Gal), and glucose (Glc), with molar ratios of 2.4:1.5:2.3:5.6:6.5. The result in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that WLSP showed a dose-dependent antiproliferative effect on the proliferation of A549 human lung cancer cells, which is consistent with the amount of lactate dehydrogenase (LDH) release from A549 cells. Prompted by this antiproliferative effect, we further examined its antiproliferative mechanism and in vivo anticancer effect. Our results showed that WLSP had the ability to cause cell cycle arrest in G1 phase, activation of caspases 3 and 9, and cleavage of poly[ADP (ribose)] polymerase (PARP) in A549 cells. The result of this in vivo study showed that WLSP could suppress the growth of xenograft A549 tumors and induce apoptosis. Taken together, these results indicate that WLSP exert an anticancer effect in vitro and in vivo and may be useful for the prevention of lung tumorigenesis.

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