Metabolic reprogramming is one of the main characteristics of malignant tumors, which is due to the flexible changes of cell metabolism that can meet the needs of cell growth and maintain the homeostasis of tissue environments. Cancer cells can obtain metabolic adaptation through a variety of endogenous and exogenous signaling pathways, which can not only promote the growth of malignant cancer cells, but also start the transformation process of cells to adapt to tumor microenvironment. Studies show that m6A RNA methylation is widely involved in the metabolic recombination of tumor cells. In eukaryotes, m6A methylation is the most abundant modification in mRNA, which is involved in almost all the RNA cycle stages, including regulation the transcription, maturation, translation, degradation and stability of mRNA. M6A RNA methylation can be involved in the regulation of physiological and pathological processes, including cancer. In this review, we discuss the role of m6A RNA methylation modification plays in tumor metabolism-related molecules and pathways, aiming to show the importance of targeting m6A in regulating tumor metabolism.

No abstract

No abstract

No abstract

No abstract

Toll-like receptors are expressed in human immune cells and many tumors, but the role of toll-like receptor 4 (TLR4) in the development of tumors is controversial. We demonstrated the expression, distribution, and functional activity of TLR4 in tissues of normal cervix, cervical intraepithelial neoplasia (CIN), invasion cervical cancers (ICC), and different human papillomavirus (HPV)-infected cervical cancer cells. The results showed that TLR4 expression was in accordance with the histopathological grade: higher in ICC than in CIN, and low in normal cervical tissues and malignant cervical stroma. Expression was higher in SiHa (HPV16+) than in HeLa (HPV18+) cells, but was not observed in C33A (HPV-) cells. After treatment with its agonist, lipopolysaccharide (LPS), the expression levels of TLR4 was increased and apoptosis resistance was induced in SiHa cells, but not in HeLa or C33A cells. Meanwhile, LPS treatment did not alter the cell cycle distribution in SiHa cells. The mechanism of apoptosis resistance may be related to HPV16 infection and not correlated with the cell cycle distribution. Targeting TLR4 in combination with traditional drug treatment may serve as a novel strategy for more effectively killing cancer cells.

Summary Texturized soybean protein (TSP) and wheat gluten were prepared at high moisture using a twin‐screw extruder. Effects of feed moisture content, extrusion temperature and wheat gluten content on the dynamic mechanical properties, microstructures and fractal analysis of texturized soybean protein/wheat gluten composite were investigated. All extruded samples were well fitted with Burger's model in creep‐recovery tests (R2 ≥ 0.978). The creep‐recovery rate decreased with an increasing extrusion temperature. The addition of wheat gluten increased the resistance to creep and the unrecoverable deformation of TSP samples. The extrusion parameters affected the microstructure and morphology of extruded products. The fractal dimension of TSP products decreased with an increase in moisture content and wheat gluten content. Texturized soybean protein (TSP) and wheat gluten composite could form well‐structure products.

Lung adenocarcinoma is the most common pathological pattern of lung cancer. During the past decades, a number of targeted agents have been explored to treat advanced lung adenocarcinoma. In the present clinical practice, antagonists of the epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF)-directed therapies are widely used. In the former category, the agent erlotinib (tyrosine kinase inhibitor) has shown obvious advantages over cytotoxic therapy. Anti-VEGF therapy bevacizumab used for lung adenocarcinoma was recommended in NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) as first-line therapy. Similarly, apatinib is speculated to response by selectively inhibiting the vascular endothelial growth factor receptor-2. The patient with unknown EGFR status benefited 5-month progressive free survival (PFS) from erlotinib, and then another 5.1-month PFS with combined treatment of apatinib, which suggested a new option for lung adenocarcinoma. However, when dabigatran was used to cancer-related venous thromboembolism during apatinib therapy, extensive subcutaneous bleeding occurred, warning us against the risks of bleeding. Besides, hypertension and anorexia were observed, causing dosage adjustment.