The morbidity and mortality of lung cancer in Xuanwei, China, are the highest in the world. This study attempts to identify differentially expressed genes (DEGs) related to lung adenocarcinoma in Xuanwei. The expression profiles of eight paired lung adenocarcinoma tissues and corresponding nontumor tissues were acquired by microarrays. Functional annotations of DEGs were carried out by bioinformatics analysis. The results of the microarrays were further verified by real-time quantitative PCR (RTq-PCR). A total of 5290 genes were classified as DEGs in lung adenocarcinoma in Xuanwei; 3325 genes were upregulated and 1965 genes were downregulated, whereas the expression of the other 11 970 genes did not change. These DEGs are involved in a wide range of cancer-related processes, which include cell division, cell adhesion, cell proliferation, and DNA replication, and in many pathways such as the p53 signaling pathway, the MAPK pathway, the Jak-STAT signaling pathway, the hedgehog signaling pathway, and the non-small-cell lung cancer pathway. The tendency of changes in the expression of 12 selected DEGs (five downregulated genes, PIK3R1, RARB, HGF, MAPK11, and SESN1, and seven upregulated genes, PAK1, E2F1, CCNE1, EGF, CDC25A, PTTG1, and UHRF1) in RTq-PCR was consistent with the expression profiling data. Expression of PAK1 was significantly increased in the low differentiation group (P=0.031), whereas expression of HGF was significantly decreased in the low differentiation group (P=0.045). RARB and MAPK11 were significantly increased in the nonsmoker group (P=0.033 and 0.040, respectively). A large number of DEGs in lung adenocarcinoma in Xuanwei have been detected, which may enable us to understand the pathogenesis and lay an important foundation for the prevention and treatment of lung adenocarcinoma in Xuanwei.

BackgroundThe lung cancer mortality rate in Xuanwei city is among the highest in China and adenocarcinoma is the major histological type. Lung cancer has been associated with exposure to indoor smoky coal emissions that contain high levels of polycyclic aromatic hydrocarbons; however, the pathogenesis of lung cancer has not yet been fully elucidated.MethodsWe performed whole genome sequencing with lung adenocarcinoma and corresponding non‐tumor tissue to explore the genomic features of Xuanwei lung cancer. We used the Molecule Annotation System to determine and plot alterations in genes and signaling pathways.ResultsA total of 3 428 060 and 3 416 989 single nucleotide variants were detected in tumor and normal genomes, respectively. After comparison of these two genomes, 977 high‐confidence somatic single nucleotide variants were identified. We observed a remarkably high proportion of C·G‐A·T transversions. HECTD4, RCBTB2, KLF15, and CACNA1C may be cancer‐related genes. Nine copy number variations increased in chromosome 5 and one in chromosome 7. The novel junctions were detected via clustered discordant paired ends and 1955 structural variants were discovered. Among these, we found 44 novel chromosome structural variations. In addition, EGFR and CACNA1C in the mitogen‐activated protein kinase signaling pathway were mutated or amplified in lung adenocarcinoma tumor tissue.ConclusionWe obtained a comprehensive view of somatic alterations of Xuanwei lung adenocarcinoma. These findings provide insight into the genomic landscape in order to further learn about the progress and development of Xuanwei lung adenocarcinoma.

We aimed to evaluate the prospective association of vitamin B5 with all-cause mortality and explore its potential modifiers in Chinese adults with hypertension. A nested, case-control study was conducted in the China Stroke Primary Prevention Trial, including 505 deaths of all causes and 505 matched controls. The median follow-up duration was 4.5 years. The primary outcome measure in this investigation was all-cause mortality, which encompassed deaths for any reason. The mean plasma vitamin B5 concentration for cases (43.7 ng/mL) was higher than that in controls (40.9 ng/mL) (p = .001). When vitamin B5 was further assessed as quintiles, compared with the reference group (Q1: < 33.0 ng/mL), the risk of all-cause mortality increased by 29%

Purpose: To investigate the function of limb bud and heart development (LBH) in 1α, 25dihydroxyvitamin D3 (1,25D)-mediated inhibitory effect on proliferation of prostate cancer cells. Methods: The inhibitory effect of 1,25D on growth and cell cycle progression of lymph node carcinoma of the prostate (LNCaP) cells was determined using cell counting kit-8 (CCK-8) assay, 5-ethynyl-2'deoxyuridine (EdU) assay and flow cytometry, while the expression levels of LBH in response to treatment with 1,25D were determined by quantitative reverse-transcription PCR (qRT-PCR) and western blottingting. The expression levels of LBH in cells were down/up regulated by transfection with siRNA or overexpression plasmids, and then cell growth and cell cycles were measured using the CCK-8 assay, EdU assay, and flow cytometry. Finally, the growth inhibitory effect of 1,25D on LBH knockdown cells were determined using CCK-8 and EdU assays. Results: Treatment with 1,25D arrested LNCaP cells in G0/G1 phase of cell cycle, suppressed the growth of the cells and induced the expression of LBH. Overexpression/knockdown of LBH in LNCaP cells suppressed/promoted cell growth and accumulated/decreased cells in the G0/G1 phase. Moreover, knockdown of LBH reversed the inhibitory effect of 1,25D on cell proliferation of LNCaP cells. Conclusion: Inhibitory effect of 1,25D on cell cycle progression and cell proliferation might be via LBH.