assessing-microglial-phagocytosis-myelin-debris-vitro-under-repeated

Assessing Microglial Phagocytosis of Myelin Debris <em>in vitro</em> Under Repeated Magnetic Stimulation

Microglia, the resident phagocytes of the central nervous system (CNS), play a pivotal role in maintaining CNS integrity and homeostasis by removing ...

Linyi People's Hospital

To study the effect of hGC-MSCs from human gastric cancer tissue on cell proliferation, invasion and epithelial-mesenchymal transition in tumor tissue of gastric cancer tumor-bearing mice.

Effect of hGC-MSCs from human gastric cancer tissue on cell proliferation, invasion and epithelial-mesenchymal transition in tumor tissue of gastric cancer tumor-bearing mice.

This study investigated the role of microRNA-95 (miR-95) in gastric cancer (GC) and to elucidate the underlying mechanism. Initially, bioinformatic prediction was used to predict the differentially expressed genes and related miRNAs in GC. miR-95 and DUSP5 expression was altered in GC cell line (MGC803) to evaluate their respective effects on the epithelial-mesenchymal transition (EMT) process, cellular processes (cell proliferation, migration, invasion, cell cycle, and apoptosis), cancer stem cell (CSC) phenotype, as well as tumor growth ability. It was further predicted in bioinformatic prediction and verified in GC tissue and cell line experiments that miR-95 was highly expressed in GC. miR-95 negatively regulated DUSP5, which resulted in the MAPK pathway activation. Inhibited miR-95 or overexpressed DUSP5 was observed to inhibit the levels of CSC markers (CD133, CD44, ALDH1, and Lgr5), highlighting the inhibitory role in the CSC phenotype. More important, evidence was obtained demonstrating that miR-95 knockdown or DUSP5 upregulation exerted an inhibitory effect on the EMT process, cellular processes, and tumor growth. Together these results, miR-95 knockdown inhibited GC development via DUSP5-dependent MAPK pathway.

microRNA-95 knockdown inhibits epithelial-mesenchymal transition and cancer stem cell phenotype in gastric cancer cells through MAPK pathway by upregulating DUSP5.

Lung cancer is the leading cause of cancer-related death worldwide, with an estimated 1.2 million deaths each year. Despite advances in lung cancer treatment, 5-year survival rates are lower than ~15%, which is attributes to diagnosis limitations and current clinical drug resistance. Recently, more evidence has suggested that epigenome dysregulation is associated with the initiation and progress of cancer, and targeting epigenome-related molecules improves cancer symptoms. Interestingly, some groups reported that the level of methylation of histone 3 lysine 4 (H3K4me3) was increased in lung tumors and participated in abnormal transcriptional regulation. However, a mechanistic analysis is not available. In this report, we found that the SET domain containing 1A (SETD1A), the enzyme for H3K4me3, was elevated in lung cancer tissue compared to normal lung tissue. Knockdown of SETD1A in A549 and H1299 cells led to defects in cell proliferation and epithelial-mesenchymal transition (EMT), as evidenced by inhibited WNT and transforming growth factor β (TGFβ) pathways, compared with the control group. Xenograft assays also revealed a decreased tumor growth and EMT in the SETD1A silenced group compared with the control group. Mechanistic analysis suggested that SETD1A might regulate tumor progression via several critical oncogenes, which exhibited enhanced H3K4me3 levels around transcriptional start sites in lung cancer. This study illustrates the important role of SETD1A in lung cancer and provides a potential drug target for treatment.

Histone methyltransferase SETD1A participates in lung cancer progression.

Pueraria Mirifica (Willd. Ohwi) is a medicine with anti-inflammatory and lipid-lowering properties. Puerarin is one of the main active components of Pueraria. The aim of this study was to investigate the possible mechanisms of Pueraria in the treatment of non-alcoholic fatty liver disease. The therapeutic effect of the drug was demonstrated by serum and liver pathology indicators. The mechanism of action of puerarin was demonstrated by intestinal microbial changes and short-chain fatty acid content tests. The mechanism of puerarin alleviating Metabolic dysfunction-associated steatotic liver disease (MASLD) by regulating intestinal flora was predicted by bioinformatics. The relationship between flora and liver was revealed by q-PCR detection of mRNA expression level of liver metabolic genes. And the mechanism of puerarin action was further verified by intestinal microbial clearance experiments. Puerarin reduced vacuolar-like changes, lipid deposition, and inflammatory cell infiltration in the livers of high-fat diet (HFD) model mice. The gut microbiota abundance and diversity were remodeled, short-chain fatty acid content was increased, and the intestinal mucosal barrier was repaired, accompanied by a reduction in inflammatory cytokines. Puerarin regulated mRNA expression of hepatic lipid metabolism genes to alleviate MASLD. These results suggested that puerarin treats MASLD by treating altering bacterial metabolism and anti-inflammation.

Article	Year
Effect of hGC-MSCs from human gastric cancer tissue on cell proliferation, invasion and epithelial-mesenchymal transition in tumor tissue of gastric cancer tumor-bearing mice. Asian Pacific journal of tropical medicine\| PubMed ID: 27569891	2016
microRNA-95 knockdown inhibits epithelial-mesenchymal transition and cancer stem cell phenotype in gastric cancer cells through MAPK pathway by upregulating DUSP5. Journal of cellular physiology\| PubMed ID: 31309567	2020
Histone methyltransferase SETD1A participates in lung cancer progression. Thoracic cancer\| PubMed ID: 34219384	2021
Puerarin improves MASLD by remodeling intestinal microenvironment to promote mitochondrial fusion and autophagy. Journal of pharmacological sciences\| PubMed ID: 40121054	2025

Mei Du

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