A new class of two-dimensional (2D) nanomaterial, transition metal dichalcogenides (TMDCs) such as MoS2, MoSe2, WS2, and WSe2 which have fantastic physical and chemical properties, has drawn tremendous attention in different fields recently. Herein, we for the first time take advantage of the great potential of MoS2 with well-engineered surface as a novel type of 2D nanocarriers for gene delivery and therapy of cancer. In our system, positively charged MoS2-PEG-PEI is synthesized with lipoic acid-modified polyethylene glycol (LA-PEG) and branched polyethylenimine (PEI). The amino end of positively charged nanomaterials can bind to the negatively charged small interfering RNA (siRNA). After detection of physical and chemical characteristics of the nanomaterial, cell toxicity was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Polo-like kinase 1 (PLK1) was investigated as a well-known oncogene, which was a critical regulator of cell cycle transmission at multiple levels. Through knockdown of PLK1 with siRNA carried by novel nanovector, qPCR and Western blot were used to measure the interfering efficiency; apoptosis assay was used to detect the transfection effect of PLK1. All results showed that the novel nanocarrier revealed good biocompatibility, reduced cytotoxicity, as well as high gene-carrying ability without serum interference, thus would have great potential for gene delivery and therapy.

Previous studies suggested that abnormal miRNA expression was a significant characteristic of malignant tumors. We aimed to explore the role of miR-106a as the potential diagnostic and prognostic biomarker in gastric cancer (GC). Firstly, the expression level of miR-106a was detected by qPCR in 28 pairs of GC cancer tissues and adjacent tissues, 48 pairs of plasma samples before and after operation from GC patients, and 22 plasma samples from healthy controls. It had revealed that the level of miR-106a in tumor tissues (2.700±2.565) was significantly higher compared to adjacent tissues (1.321±0.904) (p<0.05). Besides, the expression level of miR-106a in plasma of GC (9.479±5.595) was significantly up-regulated compared with healthy controls (2.594±2.329) (p<0.05), while a remarkable decline of miR- 106a expression was observed in plasma of GC patients after gastrectomy. Further statistic data showed high miR-106a expression was closely related to the degree of lymphatic metastasis and TNM staging of GC. We also applied ROC curve in order to evaluate miR-106a as a diagnostic marker for GC patients. As a result, the sensitivity and specificity were 60.4%, 68.2% in tissue samples and 72.9%, 63.6% in plasma samples, respectively. At last, we explored the methylation status of miR-106a promoter in 28 paired GC tissues through methylation-specific PCR (MSP), the result showed that the methylation rate was 53.6% in cancer tissues and 85.7% in adjacent tissues. Moreover, the result indicated that promoter hypomethylation of miR- 106a is related to its high expression. Our research indicated that miR-106a might serve as a potential prognostic indicator in progressive GC and up-regulated circulating miR-106a by promoter hypomethylation, might be proposed as a candidate diagnostic and prognostic indicator for GC.

Aberrant microRNA (miRNA) expression has been widely recognized to play an extremely important role in several cancers, including hepatocellular carcinoma (HCC). According to the previous studies, abnormal miR-106a expression was closely related to various cancer occurrences. However, the miR-106a expression in HCC remains unclear. In our study, we firstly detected the miR-106a expression levels in 36 pairs of HCC tissues. The results showed that miR-106a expression in HCC tissues was apparently higher than the level in the adjacent tissues. Then, we used quantitative real-time PCR (qPCR) and BSP to analyze miR-106a expression and promoter methylation in HCC cell lines. There came to a conclusion that the methylation status of the miR-106a promoter region was inversely correlated with the expression of miR-106a. After prediction with online software, we further used dual-luciferase reporter gene assay to ensure that TP53INP1 and CDKN1A might be the direct targets of miR-106a. At last, we explored the functions of miR-106a in HCC cells in vitro. Our results manifested that high-miR-106a cell line had stronger invasiveness, faster cell cycle progression, and more resistance to apoptosis compared with the low-miR-106a cell line. Therefore, our study suggested that upregulated expression of miR-106a by its promoter hypomethylation might contribute to the progression of HCC, which might be considered as a potentially effective biomarker and therapeutic approach in the future.