The aim of the study was to assess the prevalence of human papillomavirus (HPV) in the esophagus in the coastal region of Eastern Guangdong, Southern China, an area with a high incidence of esophageal carcinoma. Fresh surgical resection esophageal specimens were obtained from 176 esophageal carcinoma patients admitted to the Tumor Hospital of Shantou University Medical College. The samples were subjected to polymerase chain reaction (PCR) to detect HPV infection using consensus and type-specific primers for HPV type 6, 11, 16, and 18. The incidence rate was 65.5%, 69.1%, and 60% in tissues of cancerous, paracancerous and normal mucosa, respectively. Further analysis of the distribution of HPV types in the three sections of tissues showed that the high-risk HPV types 16 and 18 were found mainly in the cancer cells (43.2%), whereas the low-risk HPV types 6 and 11 were seen mainly in the normal mucosa (52.3%). The total infection rate of the high-risk HPV types 16 and HPV 18 was the highest in cancerous tissues (54.5%), followed by paracancerous tissues (19.5%), and the lowest in normal mucosa (11.7%). There was high incidence of HPV infection in the esophageal epithelium in Eastern Guangdong, Southern China, where esophageal carcinoma is prevalent. HPV was seen in the normal, paracancerous and cancerous tissues, with the high-risk HPV type 16 and 18 more common in cancerous tissues. The results indicate that the high incidence of esophageal carcinoma in this area is associated with HPV infection.

Background: Non-small-cell lung cancer (NSCLC) is the most prevalent cancer worldwide. Tumor microenvironment (TME) plays a very important role in the cancer development. Thus, it is urgent to find the change of TME that contributes to NSCLC carcinogenesis and progression. Methods:The bioinformatics analysis approach was applied to evaluate the change of TME and screen the differentially immune cells in NSCLC tissue based on The Cancer Genome Atlas (TCGA) data.Meanwhile, the association of differentially immune cells with tumor stage and prognosis of NSCLC was evaluated. Then, we screen the different expression genes between macrophages infiltration high group and low group. After that, the expression of LAMC2 was detected in 48 cases of NSCLC tissues and paired normal tissues. The function of LAMC2 was detected through cell experiments in vitro. Immunohistochemistry assay was used to detect the correlation between LAMC2 expression and macrophages infiltration in NSCLC tissue. LAMC2-related pathways were identified by gene set enrichment analysis.Results: Compared with early stage, middle-advanced stage of NSCLC exhibited lower immune score.Macrophages were the main component of different immune cells and correlated with poor outcome. The results of immunohistochemistry indicated that the expression of LAMC2 in NSCLC tissues was higher than paired normal tissues. Down-regulation of LAMC2 inhibited the proliferation, migration and invasion of NSCLC cells in vitro. Overexpression of LAMC2 was positively associated with macrophages infiltration in NSCLC tissues. Inhibition of LAMC2 expression in NSCLC cells could reduce THP-1 infiltration, and LAMC2 protein could promote the infiltration of THP-1. The Gene Set Enrichment Analysis results showed that high expression of LAMC2 was correlated with focal adhesion and extracellular matrix receptor interaction.Conclusions: Immune suppression and macrophages infiltration were correlated with poor outcomes in NSCLC. LAMC2 promoted macrophages infiltration and extracellular matrix remolding in NSCLC. Our studies suggested an oncogenic role of LAMC2 in NSCLC progression and it perhaps serve as a potential immune therapy target for NSCLC.

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive memory damage and cognitive dysfunction. Studies have shown that defective autophagic flux is associated with neuronal dysfunction. Modulating autophagic activity represents a potential method of combating AD. In Chinese medicine, Acori Tatarinowii Rhizoma is used to treat dementia and amnesia. β-Asarone, an active component of this rhizome can protect PC12 cells from Aβ-induced injury and modulate expression of autophagy factors. However, its cytoprotective mechanisms have yet to be discerned. It is unclear whether β-asarone affects autophagic flux and, if it does, whether this effect can alleviate Aβ cell damage. In the present study, we constructed APPswe-overexpressing PC12 cell line as a cell model of Aβ-induced damage and assessed expression of autophagic flux-related proteins as well as the number and morphology of autophagosomes and autolysosomes. Our results show that β-asarone decreases the expression levels of Beclin-1, p62, LC3-Ⅱ, and Aβ1-42. β-Asarone reduced the number of autophagosomes and increased the number of autolysosomes, as determined by confocal laser scanning microscopy and transmission electron microscopy. Our results suggest that β-asarone can protect PC12 cells from Aβ-induced damage by promoting autophagic flux, which may be achieved by enhancing autophagosome-lysosome fusion and/or lysosome function.

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