LL-37, the active product of human cathelicidin antimicrobial peptide (CAMP) has a broad spectrum of antibacterial activity. LL-37 also has important physiological functions in immune regulation, angiogenesis and in modulating apoptosis. The roles of LL-37 in oral squamous cell carcinoma (OSCC) are still not clear. The correlation between DNA methylation and human CAMP expression is also unknown. Here human CAMP/LL-37 expression was assessed by immunohistochemistry in normal and OSCC tissues. The results indicated that low expression of CAMP/LL-37 correlated with histological differentiation and lymph node metastasis and also promoted tumor progression. A cell-specific methylation pattern in the promoter region of human CAMP was detected. Treatment with 5-aza-2′-deoxycytidine, a DNA demethylation reagent can increase human CAMP expression in epithelial cancer cells. The reporter assay showed that unmethylated human CAMP promoter activity was significantly higher than methylated promoter activity. Taken together, these results suggested that human CAMP/LL-37 might act as a tumor-suppressor in OSCC and DNA methylation might play roles during carcinogenesis via directly downregulating human CAMP promoter activity.

ASCs enhanced vertical bone regeneration in calvarial defects in rats with type 2 DM, when used in association with bovine bone scaffolds. The findings suggest that a combination of ASCs and bovine bone scaffolds could improve bone quantity in vertical bone defects.

Infection with Echinococcus spp. causes fibrosis in various vital organs, including the liver and lungs. Hepatic fibrosis is a pathological feature of Echinococcus infection that destroys normal liver tissue, leading to jaundice, cholecystitis, portal hypertension, etc. Severe Echinococcus multilocularis infections lead to liver failure and hepatic encephalopathy. The formation of peripheral fiberboards around the metacestode is a major reason as to why antiparasitic drugs fail to be effectively transported to the lesion site. Studies on the mechanism of hepatic fibrosis caused by Echinococcus are important for treatment in patients. Recent studies have focused on miRNA and TGF-β. More recent findings have focused on the generation of collagen fibers around the metacestode. In this review paper we focus on the mechanism by which the Echinococcus parasite induces fibrosis in liver and some other organs in intermediate hosts—animals as well as human beings.

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Oral squamous cell carcinoma (OSCC) is one of the most common carcinomas of the oral cavity. However, the regulatory mechanisms on miR‐32‐5p remain poorly understood in OSCC. The expression of miR‐32‐5p, Krüppel‐like factor 2 (KLF2), C‐X‐C motif chemokine receptor 4 (CXCR4), and epithelial‐to‐mesenchymal transition (EMT)‐related proteins (E‐cadherin, Vimentin, N‐cadherin, and Snail) were evaluated were assessed using RT‐qPCR and Western blot. 3‐(4, 5‐Dimethylthiazolyl2)‐2, 5‐diphenyltetrazolium bromide assay, wound healing assay, and transwell assay were employed to detect cell proliferation, migration, and invasion of OSCC cells. Finally, dual‐luciferase reporter assay was performed to verify the binding relationship between KLF2 and miR‐32‐5p. MiR‐32‐5p was highly expressed while KLF2 was lowly expressed in OSCC cells, and miR‐32‐5p knockdown or KLF2 overexpression could markedly reduce cell proliferation, migration, invasion, and EMT of OSCC cells. What is more, KLF2 was the target of miR‐32‐5p, and knockdown of KLF2 abolished the inhibitory effect of miR‐32‐5p inhibitor on progression of OSCC. Finally, CXCR4 expression was negatively regulated by KLF2, and inhibition of CXCR4 obviously alleviated the biological effects of si‐KLF2 on the progression of OSCC. MiR‐32‐5p could enhance cell proliferation, migration, invasion, and EMT of OSCC cells, and the discovery of miR‐32‐5p/KLF2/CXCR4 axis might provide potential therapeutic targets for OSCC.