Of the numerous health benefits of garlic, the anticancer effect is probably the most noticeable. Observations over the past years have shown that the consumption of garlic in the diet provides strong protection against cancer risk. Previous studies involving garlic phytochemicals have usually focused on the cancer chemopreventive properties, but there is little published evidence showing its therapeutic potential in cancer treatment. In view of the multitargeted carcinoma actions and lack of severe toxicity, some components of garlic are likely to play vital roles in the selective killing of cancer cells. However, the rational design of experimental studies and clinical trials are required to verify this concept. This paper discusses the promises and pitfalls of garlic for the treatment of cancer.

Detecting bacteria at low concentrations without time-consuming culture processes would allow rapid diagnoses. Since electrostatic attraction exists between negatively charged bacterial cells and positively charged magnetic nanoparticles (NP+), capture of bacteria holds great promise towards achieving this goal. Here, we present a rapid and highly efficient approach to capture Escherichia coli, which was used as a model for gram-negative bacteria. Capture of E. coli at very low concentrations of 10 and 100 CFU/mL using NP+ is rapidly and efficiently achieved within 1 h. Moreover, the capture efficiency of NP+ was over 90% by analyzing the number of bacterial colonies on the plate. Optical and transmission electron microscopy confirmed the bacterial capture abilities of electrically charged nanoparticles (NPs). In contrast, negatively charged magnetic nanoparticles (NP−) did not show affinities towards E. coli. These results showed that bacterial cells, such as E. coli, carry a negative charge. Unlike a ligand-dependent capture system, our designed NP+ has potentials to capture a broad range of bacteria via electrostatic attractions.

Technology enabling the separation of rare circulating tumor cells (CTCs) provides the potential to enhance our knowledge of cancer metastasis and improve the care of cancer patients. Modern detection approaches commonly depend on tumor antigens or the physical size of CTCs. However, few studies report the detection of CTCs by the electrical differences between cancer cells and normal cells. In this study, we report a procedure for capturing CTCs from blood samples using electrically charged superparamagnetic nanoparticles (NPs). We found that only positively charged NPs attached to cancer cells, while negatively charged NPs did not. The capture method with positively charged NPs offered a sensitivity of down to 4 CTCs in 1 mL blood samples and achieved a superior capture yield (> 70%) for a high number of CTCs in blood samples (103–106 cells/mL). Following an in vitro evaluation, S180-bearing mice were employed as an in vivo model to assess the specificity and sensitivity of the capture procedure. The number of CTCs in blood from tumor-bearing mice was significantly higher than that in blood from healthy controls (on average, 75.8 ± 16.4 vs. zero CTCs/100 μL of blood, p < 0.0001), suggesting the high sensitivity and specificity of our method. Positively charged NPs combined with an in vivo tumor model demonstrated that CTCs can be distinguished and isolated from other blood cells based on their electrical properties.

Integrated analysis miRNA and mRNA profiling in patients with severe oligozoospermia reveals MiR-34c-3p downregulates PLDXD3 expression

Previous studies have shown that zinc-finger CCHC-type containing 13 (ZCCHC13) is located in an imprinted gene cluster in the X-inactivation centre, but few published studies have provided evidence of its expression in cancers. The CCHC-type zinc finger motif has numerous biological activities (such as DNA binding and RNA binding) and mediates protein–protein interactions. In an effort to examine the clinical utility of ZCCHC13 in oncology, we investigated the expression of the ZCCHC13 mRNA and protein in hepatocellular carcinoma (HCC). The expression of the ZCCHC13 mRNA and protein was evaluated using real-time reverse transcriptase-PCR, Western blotting and immunochemistry. DNA methylation was measured by methylation-specific PCR and bisulfite sequencing. The role of ZCCHC13 methylation was further evaluated using the demethylating agent, 5-aza-2′-deoxycytidine. The presence of anti-ZCCHC13 antibodies was determined by an ELISA. ZCCHC13 expression was frequently upregulated in human liver cancer cells and tissues. Compared with heathy individuals, sera from patients with HCC displayed a significant response to the recombinant ZCCHC13 protein. The overexpression of ZCCHC13 in HCC was attributed to DNA hypomethylation in the promoter region. Moreover, overexpression of ZCCHC13 in liver cancer cells promoted cell cycle progression by facilitating the G1-S transition, which was related to aberrant activation of the ATK/ERK/c-MYC/CDK pathway. Based on our findings, ZCCHC13 functions an oncogene for HCC, and DNA hypomethylation is a driving factor in carcinogenesis.

The objective of this study was to identify genes regulated by methylation that were involved in spermatogenesis failure in non-obstructive azoospermia (NOA). Testis biopsies of patients with NOA and OA (with normal spermatogenesis) were evaluated by microarray analysis to examine DNA methylation and mRNA expression using our established integrative approach. Of the coordinately hypermethylated and down-regulated gene list, zinc-finger CCHC-type containing 13 (ZCCHC13) was present within the nuclei of germ cells of testicular tissues according immunohistochemistry, and there was decreased protein expression in men with NOA compared with OA controls. Mechanistic analyses indicated that ZCCHC13 increased c-MYC expression through the p-AKT and p-ERK pathways. To confirm the changes inZCCHC13expression in response to methylation, 5-aza-2′-deoxycitidine (5-Aza), a hypomethylating agent, was administered to mouse spermatogonia GC-1 cells. We demonstrated that 5-Aza enhanced protein and mRNA expression ofZCCHC13epigenetically, which was accompanied by activation of p-AKT and p-ERK signaling. Our data, for the first time, demonstrate that ZCCHC13 is an important signaling molecule that positively regulates the AKT/MAPK/c-MYC pathway and that methylation aberrations ofZCCHC13may cause defects in testis development in human disease, such as NOA.