Regulation of the TUG1/miR-145-5p/SOX2 axis on the migratory and invasive capabilities of melanoma cells.

Melanoma is the most prevalent malignancy of cutaneous carcinomas. Taurine-upregulated gene 1 (TUG1), a lncRNA, is a pivotal regulator of cutaneous malignancies. The present study aimed to investigate the impact and possible mechanisms of action of TUG1 behind the progression of melanomas. Reverse transcription-quantitative PCR was conducted to detect the expression levels of TUG1, microRNA (miR)-145-5p and SOX2 in melanoma tissues and cell lines. Cell Counting Kit-8 (CCK-8) assays were performed to measure the proliferative ability of melanoma cells and transwell assays were used to examine the migration and invasion of melanoma cells. Dual luciferase reporter and RNA immunoprecipitation (RIP) assays were utilized to identify the interactions among TUG1, miR-145-5p and SOX2. Western blotting and immunohistochemical assays were performed to determine the expression profile of SOX2. The impact of TUG1 on melanoma tumorigenesis was assessed using tumorigenicity assays. TUG1 expression levels were elevated in melanoma tumor tissues and cell lines. Reduced TUG1 expression levels significantly inhibited the proliferative, migratory and invasive abilities of melanoma cells. The expression levels of miR-145-5p were decreased in melanoma tumor tissues and cell lines. TUG1 directly targeted miR-145-5p and downregulated miR-145-5p. Upregulation of TUG1 counteracted the promotion of the proliferative, migratory and invasive abilities of melanoma cells induced by the overexpression of miR-145-5p. SOX2 was a target of miR-145-5p and its expression was negatively regulated by miR-145-5p, while positively regulated by TUG1. TUG1 regulated SOX2 expression through sponging miR-145-5p. Silencing of TUG1 also inhibited melanoma tumorigenesis in mice. In conclusion, the TUG1/miR-145-5p/SOX2 axis regulated the migration and invasion of melanoma cells.

Circular RNA hsa_circ_0043688 serves as a competing endogenous RNA for microRNA-145-5p to promote the progression of Keloids via Fibroblast growth factor-2.

BACKGROUND: Keloids are benign fibroproliferative skin tumors. Circular RNA (circRNA) hsa_circ_0043688 has been exhibited to the freakishly expressed in keloid tissues. Here, we aimed to investigate the regulatory network of hsa_circ_0043688 in the pathological process of keloid. METHODS: Hsa_circ_0043688, microRNA-145-5p (miR-145-5p), and Fibroblast growth factor-2 (FGF2) level were detected using RT-qPCR. Cell viability, proliferation, apoptosis, invasion, and migration were investigated using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, transwell, and wound healing assays, respectively. Western blot analysis of protein levels of FGF2, CyclinD1, Collagen I, and Collagen III. After the prediction of Circinteractome and Starbase, their interaction was verified based on a dual-luciferase reporter and RIP assays. RESULTS: Increased hsa_circ_0043688 and FGF2, and decreased miR-145-5p in keloids samples and fibroblasts were found. Also, hsa_circ_0043688 absence hindered proliferation, invasion, migration, and boost apoptosis of keloid fibroblasts. In mechanism, hsa_circ_0043688 modulated FGF2 content via sponging miR-145-5p. CONCLUSION: Hsa_circ_0043688 knockdown inhibited cell growth and metastasis of keloid fibroblasts via miR-145-5p/FGF2, providing a new mechanism to understand the keloid progression.

Thymol improves salinity tolerance of tobacco by increasing the sodium ion efflux and enhancing the content of nitric oxide and glutathione.

BACKGROUND AND OBJECTIVE: Salt stress is one of the most important abiotic stresses affecting the yield and quality of tobacco (Nicotiana tabacum). Thymol (a natural medicine) has been widely used in medical research because of its antibacterial and anti-inflammatory activities. However, the influence of thymol on the root growth of tobacco is not fully elucidated. In this study, the regulatory effects of different concentrations of thymol were investigated. METHODOLOGY: Here, histochemical staining and biochemical methods, non-invasive micro-test technology (NMT), and qPCR assay were performed to investigate the effect of thymol and mechanism of it improving salinity tolerance in tobacco seedlings. RESULTS: In this study, our results showed that thymol rescued root growth from salt stress by ameliorating ROS accumulation, lipid peroxidation, and cell death. Furthermore, thymol enhanced contents of NO and GSH to repress ROS accumulation, further protecting the stability of the cell membrane. And, thymol improved Na+ efflux and the expression of SOS1, HKT1, and NHX1, thus protecting the stability of Na+ and K+. CONCLUSION: Our study confirmed the protecting effect of thymol in tobacco under salt stress, and we also identified the mechanism of it, involving dynamic regulation of antioxidant system and the maintenance of Na+ homeostasis. It can be a new method to improve salinity tolerance in plants.