Previous studies have indicated that certain microRNAs (miRNAs/miRs) function as either tumor suppressors or oncogenes in human cancer. The present study identified the miR-23a/27a/24-2 cluster, containing miR-23, miR-27a and miR-24, as an oncogene in gastric cancer. The expression of the miR-23a/27a/24-2 cluster was upregulated in clinical gastric cancer tissues. Transfection with inhibitors of miR-23a, miR-27a, or miR-24, either independently or together, repressed in vitro colony formation and in vivo tumor formation. The miR23a/27a/24-2 cluster inhibitors repressed the growth of gastric cancer cells in a synergistic manner. In addition, treatment with lower doses of the miRNA inhibitor mixture induced the formation of apoptotic bodies. According to computational predictions using TargetScan, suppressor of cytokine-induced signaling 6 (SOCS6) was identified as one of the downstream target genes of the miR-23a/27a/24-2 cluster. The expression of SOCS6 was significantly lower in tumor tissues than in matched normal tissues (P<0.01) and was associated with poor survival (P<0.00001). Taken together, these results strongly suggested that the miR-23a/27a/24-2 cluster may mediate the progression of gastric cancer through the suppression of SOCS6 expression. The present study also provides a novel molecular target for the development of an anti-gastric cancer agent.

Micro RNA s (mi RNA s) are confirmed to be tumor promoters or suppressors in multiple squamous cell carcinomas ( SCC s). miR‐99a‐5p has been demonstrated to be downregulated in cancerous tissues, but its functional role in head and neck SCC ( HNSCC ) and its mechanism of action have not been fully elucidated. Here, we studied the expression of miR‐99a‐5p in HNSCC and performed a clinical value assessment and then extracted mature expression data from The Cancer Genome Atlas ( TCGA ) and microarrays from Gene Expression Omnibus ( GEO ). Furthermore, biological analysis was constructed via online prediction tools. The results revealed that miR‐99a‐5p expression was markedly lower in HNSCC tissues than in normal tissues, which also showed significance in the prognosis of HNSCC . However, its diagnostic value could not be verified due to the lack of body fluid samples. Additionally, miR‐99a‐5p was expressed at higher levels in patients with low histological grade neoplasms than those with high histological grade neoplasms. The age of the patient might also be a possible clinical parameter affecting miR‐99a‐5p expression. Furthermore, miR‐99a‐5p significantly influenced HNSCC progression by regulating the PI 3K‐Akt signaling pathway, in which the key target genes were upregulated in 519 HNSCC tissues compared to 44 normal tissues, as determined by the Gene Expression Profiling Interactive Analysis ( GEPIA ). In conclusion, our study may provide insights into the expression and mechanism of miR‐99a‐5p in HNSCC . Further studies are required to elucidate the role of miR‐99a‐5p and its potential clinical applications for HNSCC .

Patients with esophageal carcinoma (ESCA) have a poor prognosis and high mortality rate. Although standard therapies have had effect, there is an urgent requirement to develop novel options, as increasing drug tolerance has been identified in clinical practice. In the present study, differentially expressed genes (DEGs) of ESCA were identified in The Cancer Genome Atlas and Genotype-Tissue Expression databases. Functional and protein-protein interaction (PPI) analyses were performed. The Connectivity Map (CMAP) was selected to predict drugs for the treatment of ESCA, and their target genes were acquired from the Search Tool for Interactions of Chemicals (STITCH) by uploading the Simplified Molecular-Input Line-Entry System structure. Additionally, significant target genes and ESCA-associated hub genes were extracted using another PPI analysis, and the corresponding drugs were added to construct a network. Furthermore, the binding affinity between predicted drug candidates and ESCA-associated hub genes was calculated using molecular docking. Finally, 827 DEGs (|log2 fold-change|≥2; q-value <0.05), which are principally involved in protein digestion and absorption (P<0.005), the plasminogen-activating cascade (P<0.01), as well as the ‘biological regulation’ of the Biological Process, ‘membrane’ of the Cellular Component and ‘protein binding’ of the Molecular Function categories, were obtained. Additionally, 11 hub genes were obtained from the PPI network (all degrees ≥30). Furthermore, the 15 first screen drugs were extracted from CMAP (score <−0.85) and the 9 second screen drugs with 70 target genes were extracted from STITCH. Furthermore, another PPI analysis extracted 51 genes, and apigenin, baclofen, Prestwick-685, menadione, butyl hydroxybenzoate, gliclazide and valproate were selected as drug candidates for ESCA. Those molecular docking results with a docking score of >5.52 indicated the significance of apigenin, Prestwick-685 and menadione. The results of the present study may lead to novel drug candidates for ESCA, among which Prestwick-685 and menadione were identified to be significant new drug candidates.

Negative differential resistance (NDR) with multi‐level resistive switching has been investigated for realizing multi‐level memory devices. However, achieving a high peak‐to‐valley ratio of NDR is a formidable challenge for a reliable multi‐level switch. Here, a new type of a light‐enhanced NDR device accompanied with resistive switching based on glutamine‐functionalized MoS2 quantum dots has been demonstrated. By increasing the illuminated light power on the device, the NDR effect can be greatly enhanced and a peak‐to‐valley ratio as high as 15.5 has been achieved. The tunneling transport and carrier trapping of the interface states are responsible for the mechanism of the light‐enhanced NDR. Multi‐level resistive switching can be realized in the same device by adjusting the illuminated light power. A high on/off resistance ratio of ≈103 and good endurance in multi‐valued switching have been achieved, exhibiting potential applications in multi‐level memory devices.