The kidney is one of the most commonly damaged organs in sepsis. Acute kidney injury (AKI) induced by sepsis is a clinically dangerous disease with a high mortality rate. Therefore, it is particularly important to find a way to prevent and treat sepsis-induced AKI.
 
  Human renal tubular epithelial cell line (HK-2) and 8-week-old C57BL/6 mice were used.  https://www.selleckchem.com/products/diphenhydramine.html  Lipopolysaccharide (LPS) was used to induce HK-2 cell injury and mouse AKI. Lentiviruses overexpressing TRIM27 were constructed to increase TRIM27 expression in HK-2 cells. Then, the effects of TRIM27 on the inflammation and apoptosis of HK-2 cells were analyzed, and those of TRIM27 recombinant protein on AKI in mice was detected by immunohistochemical staining and Western blot.
 
  It was found that TRIM27 overexpression reduced the expressions of inflammatory factors and signaling molecules in apoptosis-related pathways in HK-2 cells, but increased the ratio of Bcl-2 to Bax in HK-2 cells, indicating the anti-apoptotic effect of TRIM27. Toll-like receptor 4 (TLR4)/NF-κB signaling pathway is an important mechanism of LPS mediated renal injury, and TRIM27 overexpression in HK-2 cells significantly inhibited the activity of TLR4/NF-κB signaling pathway. In addition, AKI was significantly relieved in mice treated with TRIM27 recombinant.
 
  TRIM27 exerts anti-inflammatory and anti-apoptotic effects by inhibiting the TLR4/NF-κB signaling pathway, which effectively alleviates LPS-induced HK-2 cell damage and mouse AKI.
 TRIM27 exerts anti-inflammatory and anti-apoptotic effects by inhibiting the TLR4/NF-κB signaling pathway, which effectively alleviates LPS-induced HK-2 cell damage and mouse AKI.
  CircRNAs are vital factors involved in the pathological processes. This study aims to elucidate the biological functions of hsa_circ_0000337 in affecting the malignant progress of glioma.
 
  Relative levels of hsa_circ_0000337 in 45 cases of glioma and 24 cases of normal tissues were tested. The correlation between hsa_circ_0000337 and clinical features of glioma was assessed. Proliferative and metastatic abilities of U87 and U251 cells regulated by hsa_circ_0000337 were examined by 5-Ethynyl-2'-deoxyuridine (EdU) and transwell assay, respectively. Potential molecular mechanism of hsa_circ_0000337 on regulating glioma cell functions was clarified by bioinformatic analysis, which was further verified through rescue experiments.
 
  Hsa_circ_0000337 was highly expressed in glioma cases. Its level was correlated to poor prognosis of glioma. In vitro experiments obtained the conclusion that hsa_circ_0000337 accelerated proliferative and metastatic abilities of glioma cells. Serving as a ceRNA, hsa_circ_0000337 sponged miRNA-942-5p to upregulate MAT2A, thus inducing the malignant phenotypes of glioma.
 
  Hsa_circ_0000337/miRNA-942-5p / MAT2A axis is responsible for the deterioration of glioma. Hsa_circ_0000337 may be a potential therapeutic target for glioma.
 Hsa_circ_0000337/miRNA-942-5p / MAT2A axis is responsible for the deterioration of glioma. Hsa_circ_0000337 may be a potential therapeutic target for glioma.
  We aimed at investigating the expression levels of SET7/9 in glioma and the relationship between SET7/9 and LncRNA DRAIC. Further, we explored the relationship between SET7/9 and glioma cell metastasis and mood.
 
  The expression levels of DRAIC and miR-18a-3p in gastric cancer cells were measured by quantitative polymerase chain reaction (qPCR). The binding site of the promoter of DRAIC by H3K4me3 was confirmed by ChIP-Real-time PCR. The direct target of DRAIC and miR-18a-3p in gastric cancer cells was measured by a Luciferase reporter assay. Cell proliferation was detected by Cell counting kit-8 (CCK8), and cell invasion and migration were measured by transwell assays.
 
  Compared with adjacent non-cancerous normal tissues, SET7/9 and DRAIC were both downregulated and miR-18a-3p was upregulated in glioma cells. Meanwhile, silencing of SET7/9 enhanced cell proliferation, migration, and invasion in U251 cells. H3K4me3 protein can bind to DRAIC promoter directly. Inhibition of SET7/9 and downregulation of DRAIRAIC promoter regulated the growth and metastasis of glioma cells by targeting miR-18a-3p. It potentially provides a new therapeutic marker targeting glioma.
  This study was designed to investigate the role of microRNA-198 in thyroid cancer (TCa) progression.
 
  Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to examine microRNA-198 and H3F3A levels in tumor tissue specimens and paracancerous ones collected from 50 patients with TCa, and the interplay between microRNA-198 or H3F3A and some clinical indicators or prognosis of TCa patients was analyzed as well. MicroRNA-198 and H3F3A overexpression models were constructed using lentivirus in TCa cell lines TPC-1 and BHP2-7, and the impacts of microRNA-198 on TCa cell functions were evaluated by using cell counting kit-8 (CCK-8), plate clone formation, and transwell assays. Finally, recovery investigations were conducted to explore the underlying mechanisms as well as the interaction between microRNA-198 and H3F3A.
 
  QRT-PCR indicated that in tumor tissues of TCa patients, microRNA-198 showed a remarkably lower expression than in adjacent normal tissue samples. Compared with patients with h malignant progression of TCa by regulating H3F3A. Meanwhile, microRNA-198 is remarkably associated with pathological stage, tumor size, lymph node metastasis, and poor prognosis of TCa.
 MicroRNA-198 is remarkably reduced in TCa and inhibits malignant progression of TCa by regulating H3F3A. Meanwhile, microRNA-198 is remarkably associated with pathological stage, tumor size, lymph node metastasis, and poor prognosis of TCa.
  The aim of this study is to uncover the correlations of the expression of colon cancer associated transcript 2 (CCAT2) in the clinical papillary thyroid carcinoma (PTC) and anaplastic thyroid carcinoma (ATC) specimens with the prognosis and chemoresistance of patients.
 
  The expression level of CCAT2 in the PTC and ATC specimens was determined using Real-Time quantitative Polymerase Chain Reaction (RT-qPCR), and the correlations of CCAT2 expression with the clinical features of patients were detected via χ2 test. Besides, survival analysis was conducted to verify the relation between CCAT2 expression and patients' survival. After knockdown or overexpression of CCAT2, the changes in the proliferation ability of human thyroid carcinoma cells were examined via Cell Counting kit-8 (CCK-8) assay, and the half maximal inhibitory concentration (IC50) values of doxorubicin and cisplatin were measured by methyl thiazolyl tetrazolium (MTT) assay.
 
  According to the χ2-test results, the expression of CCAT2 was notably correlated with the capsular invasion and lymph node metastasis of PTC, and the capsular invasion, tumor size, and lymph node metastasis of ATC.