CCL18 Knockdown Suppresses Cell Growth and Migration in Thyroid Cancer.

BACKGROUND: Chemokine (C-C motif) ligand 18 (CCL18) is a chemokine that plays a key role in immune and inflammatory responses. In recent years, CCL18 participates in the development and progression of various cancers, but its expression and role in thyroid cancer (TC) remain unclear. METHODS: RT-qPCR assay and Western blot assay were used to explore the expression level of CCL18 in TC tissues and cells. Cell proliferation was measured by MTT assay. Transwell assay was adopted to detect cell migration in TC cells. Dual luciferase reporter assay was performed to assess the relationship between CCL18 and miR-149-5p. RESULTS: There was an uptrend of CCL18 in TC tissues and cells. Our findings indicated that CCL18 overexpression facilitated lymph node metastasis in patients with TC. CCL18 silencing was found to inhibit cell migration, proliferation, and EMT progression in TC cells. CCL18 was proved to be a target gene of miR-149-5p. Additionally, miR-149-5p weakened the effect of CCL18 in the progression of TC. CONCLUSION: Therefore, our results indicated that CCL18 knockdown restrained TC progression and suggested that CCL18 might be a potential therapeutic target for TC.

MiR-181a promotes cell proliferation and migration through targeting KLF15 in papillary thyroid cancer

IntroductionPapillary thyroid cancer (PTC) is the predominant histological type of thyroid cancer, accounting for 80% of thyroid cancers. MiR-181a is a novel microRNA that is usually upregulated in multiple cancers. This study aims to explore the role and underlying mechanism of miR-181a in PTC.MethodsCCK8 and Transwell assays were performed to evaluate cell viability and migration. The mRNA level of miR-181a and KLF15 was calculated by qRT-PCR. The protein level of E-Cadherin, N-Cadherin and GAPDH was evaluated by western blot. Dual luciferase assay was conducted to validate that miR-181a directly targeting the 3′-UTR of KLF15 mRNA in TPC-1 cells.ResultsWe observed that miR-181a was overexpressed and KLF15 was low expressed in PTC tissues and cell lines. Upregulation of miR-181a or downregulation of KLF15 predicted poor outcomes in PTC patients. MiR-181a improved cell growth of PTC, migration and epithelial–mesenchymal transition (EMT) in TPC-1 cells. KLF15 was a target gene of miR-181a and its expression was mediated by miR-181a. KLF15 partially reversed the facilitating effect of miR-181a on cell proliferation and migration in TPC-1 cells.ConclusionWe discovered that miR-181a served as an oncogene downregulating KLF15, thereby inhibiting cell proliferation, migration and the EMT. These findings demonstrate that miR-181a plays a significant role in PTC progression and could be a therapeutic target for PTC.

Tree root-inspired robust superhydrophobic coatings with high permeation for porous structures.

Superhydrophobic coatings have tremendous potential for protecting porous structures from corrosion. However, the weak adhesion and poor abrasion resistance have long been challenges for their real-life applications. Inspired by tree roots, we prepared a robust superhydrophobic coating by spraying fluorinated nanodiamonds (FNDs) on a permeable epoxy coating. The epoxy can not only coat the surface but also permeate deeply inside a porous substrate and consolidate in situ as tree roots in soil. Thus, the structure is thoroughly reinforced where the pull-off strength reaches 9.4 MPa for concrete. On the other hand, the surface is covered with immobilized FNDs, forming a superhydrophobic surface. Thanks to the ultra-hard FNDs, the coating surface has high abrasion resistance and its superhydrophobicity holds even after 100 abrasion cycles. Moreover, it exhibits self-cleaning, anti-icing, and anticorrosion performance. It is promising in protecting various porous structures such as concrete, wood, and untreated corroded steel.

Comparison of Transcriptome Between Type 2 Diabetes Mellitus and Impaired Fasting Glucose.

BACKGROUND The aim of this study was to compare the transcriptome between impaired fasting glucose (IFG) and type 2 diabetes mellitus (T2DM), and further research their molecular mechanisms. MATERIAL AND METHODS The original microarray GSE21321, including miRNA and mRNA expression profiles, was downloaded from the GEO database. Data preprocessing was processed by limma package, and differentially expressed genes (DGs) and miRNA (DMs) were screened. Then, the regulatory relationships among miRNA, TF, and genes were screened and the regulatory network was constructed. Finally, DAVID was used for KEGG enrichment analysis. RESULTS There were 11 upregulated IFG-related DMs and five upregulated T2DM-related DMs. Three of the DMs overlapped. In addition, there were eight downregulated IFG-related DMs and two downregulated T2DM-related DMs. Only one downregulated DM overlapped. Similarly, there were 264 upregulated IFG-related DGs and 331 upregulated T2DM-related DGs; and 196 overlapping genes were obtained. In addition, there were 400 downregulated IFG-related DMs and 568 downregulated T2DM-related DMs. A total of 326 downregulated DMs were overlapped. The overlapped DGs were enriched in various pathways, including hematopoietic cell lineage, Fc gamma R-mediated phagocytosis, and MAPK signaling pathway. TAF1 (upregulated gene) and MAFK (downregulated gene) were hub nodes both in IFG- and T2DM-related miRNA-TF-gene regulatory network. In addition, miRNAs, including hsa-miR-29a, hsa-miR-192, and hsa-miR-144, were upregulated hub nodes in the two regulatory networks. CONCLUSIONS Genes including TAF1 and MAFK, and miRNAs including hsa-miR-29a, hsa-miR-192, and hsa-miR-144 might be potential target genes and important miRNAs for IFG and T2DM.

Differential expression network analysis for diabetes mellitus type 2 based on expressed level of islet cells.

OBJECTIVE: Diabetes mellitus type 2 (T2DM) is a metabolic disease that has become a pressing issue, with potential adverse impact on mental health. We aimed to explore the potential molecular mechanism of T2DM. MATERIAL AND METHODS: GSE38642 microarray data downloaded from gene expression omnibus was used to identify the differentially expressed genes (DEGs). Profiling of complex functionality (ProfCom) was used to analyze the complex function and mine T2DM signature genes. Finally, the differential expression network (DEN) was constructed. RESULTS: We identified 147 DEGs including 59 up- and 88 down-regulated genes. With increasing of degree, the specificity of functional description of DEGs was higher. GO term of "integral to membrane and immune response (not receptor activity) not regulation of immune response" in degree 4 was enriched by 6 DEGs, while the GO term of "immune response" in degree 1 was enriched by 12 DEGs. Two complex functions of integral to membrane an immune response and response to glucose stimulus were enriched by 11 T2DM signature genes including ARG2, GLP1R, PFKFB2, PTPRN, ACSL5, CCR7, IL2RA, IL7R, IL1R2, IL1RL1 and CHST4. Finally, DEN including 11 signature genes and 491 edges was obtained. CONCLUSION: The identified DEGs especially 11 signature genes such as PTPRN, GLP1R, CCR7 and IL2RA may play important roles in the pathogenesis of T2DM.

Effects of preventative application of metformin on bile acid metabolism in high fat-fed/streptozotocin-diabetic rats.

OBJECTIVE: This study was designed to investigate the effects of metformin on bile acid in type 2 diabetes mellitus (T2DM). METHODS: In this study, we constructed a model of T2DM by a combination of high-fat diet (HFD) and low dose of streptozotocin (STZ) intraperitoneal injection. Blood samples by tail vein and eye angular vein were withdrawn before (time 0) and 30, 60, and 120 minutes after administration of glucose before STZ injection and once a week after diabetes induction, and were analyzed to evaluate the level of the fasting blood glucose and fasting insulin using glucometer. Triglyceride, low density lipoprotein cholesterin, high density lipoprotein cholesterin were detected by automatic biochemical analyzers. Total cholesterol and total bile acid (TBA) were analyzed using ELISA kits. RESULTS: Before STZ injection, the TBA level in HFD group was significantly higher relative to that in standard diet (SD) group and there was a moderate reduction of the TBA level in early intervention (EI) group 6 week after metformin administration comparing with that in HFD group but was still higher than that of SD group. However, after STZ injection, the TBA level was significantly higher in DM rats relative to that in normal control (NC) rats and the TBA level in late intervention (LI) (19.92 µmol/L) and EI rats (42.97 µmol/L) with metformin administration was significantly higher comparing with that in DM rats. CONCLUSION: The effects of metformin in plasma glucose and lipid metabolism might be associated with bile acid metabolism.