Fang Li

Abstract Long noncoding RNAs (lncRNA) have been shown to play critical roles in many diseases, including esophageal squamous cell carcinoma (ESCC). Recent studies have reported that some lncRNA encode functional micropeptides. However, the association between ESCC and micropeptides encoded by lncRNA remains largely unknown. In this study, we characterized a Y-linked lncRNA, LINC00278, which was downregulated in male ESCC. LINC00278 encoded a Yin Yang 1 (YY1)-binding micropeptide, designated YY1BM. YY1BM was involved in the ESCC progression and inhibited the interaction between YY1 and androgen receptor (AR), which in turn decreased expression of eEF2K through the AR signaling pathway. Downregulation of YY1BM significantly upregulated eEF2K expression and inhibited apoptosis, thus conferring ESCC cells more adaptive to nutrient deprivation. Cigarette smoking decreased m6A modification of LINC00278 and YY1BM translation. In conclusion, these results provide a novel mechanistic link between cigarette smoking and AR signaling in male ESCC progression. Significance: Posttranscriptional modification of a micropeptide-encoding lncRNA is negatively impacted by cigarette smoking, disrupting negative regulation of the AR signaling pathway in male ESCC.

Native silk features strong, extensible and tough properties which originate from its hierarchical nanofibril structure. In the present study, native silk nanofibrils were obtained by dissolving degummed silk in salt–formic acid (FA), such as CaCl2–FA. The CaCl2–FA dissolved silk by breaking hydrogen bonds in the crystalline region while preserving the nanofibril structures. The dissolution behavior of silk from fibre to nanofibril was determined by Na2CO3 concentration during the degumming process, and was regulated by CaCl2 concentration during the dissolution process. The resulting solution containing silk fibroin (SF) nanofibrils could be easily processed into films with nanofibrous structures and high strength. In addition, high-quality electrospun SF nanofibres could also be generated easily from this solution. The novel dissolution and regeneration behavior of silk at the nanofibril scale provides new insights into methods for the preparation of high-quality silk materials for application in high-tech areas.

High-performance and useful graphene oxide (GO) and cellulose nanocrystals (CNCs) are easily extracted from natural graphite and cellulose raw materials, and poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) is produced by bacterial fermentation from natural plant corn stalks, etc. In this study, novel ternary nanocomposites consisting of PHBV/cellulose nanocrystal-graphene oxide nanohybrids were prepared via a simple solution casting method. The synergistic effect of CNC with GO nanohybrids obtained by chemical grafting (CNC-GO, covalent bonds) and physical blending (CNC/GO, noncovalent bonds) on the physicochemical properties of PHBV nanocomposites was evaluated and the results compared with a single component nanofiller (CNC or GO) in binary nanocomposites. More interestingly, ternary nanocomposites displayed the highest thermal stability and mechanical properties. Compared to neat PHBV, the tensile strength and elongation to break increased by 170.2 and 52.1%, respectively, and maximum degradation temperature (Tmax) increment by 26.3 °C, were observed for the ternary nanocomposite with 1 wt % covalent bonded CNC-GO. Compared to neat PHBV, binary, and 1:0.5 wt % noncovalent CNC/GO based nanocomposites, the ternary nanocomposites with 1 wt % covalent bonded CNC-GO exhibited excellent barrier properties, good antibacterial activity (antibacterial ratio of 100.0%), reduced barrier properties, and lower migration level for both food simulants. Such a synergistic effect yielded high-performance ternary nanocomposites with great potential for bioactive food packaging materials.

Inhibitory costimulatory molecule CD274 expresses in various cancers and contributes to cancer immune evasion by inhibiting T cell activation and proliferation, yet the regulatory mechanisms for CD274 overexpression in cancers are poorly understood. In this study, we discovered a novel mechanism of CD274 expression regulated by miR-570. A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 overexpression by disrupting the miR-570 binding. The mutations were widely observed in cancers by sequencing of 276 gastrointestinal cancers (esophageal, gastric, colorectal, hepatocellular, and pancreatic cancers). This mutation was significantly associated with CD274 overexpression in gastric cancer (P = 1.44×10(-10)) and with the pathological features including differentiation grade, depth of tumor invasion, lymph node metastasis, and tumor-node-metastases (TNM) stage. These findings suggest a novel regulatory mechanism for CD274 overexpression in gastric cancer mediated by miR-570 and a somatic mutation in CD274 3'-UTR, and provide a new insight to gastric carcinogenesis.