Alterations of gut microbiota and its correlation with the liver metabolome in the process of ameliorating Parkinson's disease with Buyang Huanwu decoction.

Ethnopharmacological Relevance: Buyang Huanwu decoction (BHD), a famous traditional Chinese medicine (TCM) formula, was first recorded in Qing Dynasty physician Qingren Wang's Yi Lin Gai Cuo. BHD has been widely utilized in the treatment of patients with neurological disorders, including Parkinson's disease (PD). However, the underlying mechanism has not been fully elucidated.

Integrated analysis of metabolomic and transcriptomic profiling reveals the effect of Buyang Huanwu decoction on Parkinson's disease in mice.

Background: Parkinson's disease (PD) is a common, complex, and chronic neurodegenerative disorder involved in multi-system. At present, medicine for PD has many limitations. Buyang Huanwu decoction (BHD), a famous traditional Chinese medicinal (TCM) formulae, is used in the treatment of PD clinically in China.

Multi-Omics Reveals Inhibitory Effect of Baicalein on Non-Alcoholic Fatty Liver Disease in Mice.

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, whose etiology is poorly understood. Accumulating evidence indicates that gut microbiota plays an important role in the occurrence and progression of various human diseases, including NAFLD. In this study, NAFLD mouse models were established by feeding a high-fat diet (HFD).

Effects and Mechanisms of Saikosaponin D Improving the Sensitivity of Human Gastric Cancer Cells to Cisplatin.

Gastric cancer (GC) is the second leading cause of cancer deaths around the world. Chemoresistance is an important reason for poor prognosis of GC. Saikosaponin D (SSD) is a natural constituent from and exhibits various activities including antitumors.

Importin β1 mediates nuclear import of the factors associated with nonsense-mediated RNA decay.

In eukaryotic cells, nonsense-mediated RNA decay (NMD) is an essential physiological mechanism coupled to translation, regulating the stability of abnormal RNA containing premature termination codon (PTC) and a significant fraction of normal transcriptomes. So far, the molecular regulation mechanism of NMD pathway is far from fully elucidated. Previously, we observed the interaction between importin β1 (Impβ1) and UPF1, a core factor of NMD.

Baicalein enhanced cisplatin sensitivity of gastric cancer cells by inducing cell apoptosis and autophagy via Akt/mTOR and Nrf2/Keap 1 pathway.

Baicalein is a natural flavonoid with various pharmacological activities including antitumor. The synergistic anti-cancer effect of the combination of baicalein and Cisplatin (DDP) on gastric cancer (GC) has not been reported. MTT assay and colony formation assay were used to determine the inhibitory effect of the combination of baicalein and DDP on cell survival.

MARVELD1 regulates integrin β1-mediated cell adhesion and actin organization via inhibiting its pre-mRNA processing.

Cell adhesion on an extracellular matrix (ECM) participates in cell motility, invasion, cell signal transduction and gene expression. Many nuclear proteins regulate cell-ECM adhesion through managing the transcription of cell adhesion-related genes. Here, we identified MARVEL [MAL (The myelin and lymphocyte protein) and related proteins for vesicle trafficking and membrane link] domain containing 1 (MARVELD1) that could suppress cell spreading and complicate actin organization.

MARVELD1 Inhibits Nonsense-Mediated RNA Decay by Repressing Serine Phosphorylation of UPF1.

We have observed low expression levels of MARVELD1, a novel tumor repressor, in multiple tumors; however, its function in normal cells has not been explored. We recently reported that MARVELD1 interacts with importin β1, which plays an important role in nonsense-mediated RNA decay(NMD). Here, we demonstrate that MARVELD1 substantially inhibits nonsense-mediated RNA decay by decreasing the pioneer round of translation but not steady-state translation, and we identify MARVELD1 as an important component of the molecular machinery containing UPF1 and Y14.

Down expression of LRP1B promotes cell migration via RhoA/Cdc42 pathway and actin cytoskeleton remodeling in renal cell cancer.

The low-density lipoprotein receptor-related protein 1B (LRP1B) is known as a putative tumor suppressor. The decreased expression of LRP1B has been involved in multiple primary cancers in several studies. However, its expression and function in the carcinogenesis of renal cell cancer (RCC) remain unclear.

MARVELD1 inhibited cell proliferation and enhance chemosensitivity via increasing expression of p53 and p16 in hepatocellular carcinoma.

We have previously found that expression of MARVELD1 was remarkably downregulated in multiple tumor tissues, but unclear in hepatocellular carcinoma (HCC) and its function has not been explored yet. In the present study, to uncover the underlying mechanism of MARVELD1 in the pathogenesis and development of HCC, we investigated the expression pattern of MARVELD1 and its effect on tumor proliferation in HCC. The results indicated the frequent downregulation of MARVELD1 in clinic samples and cell lines of HCC resulted from promoter methylation, as well as genetic deletion.

Identification and characterization of MARVELD1, a novel nuclear protein that is down-regulated in multiple cancers and silenced by DNA methylation.

MARVELD1 (MARVEL domain-containing 1) is a member of MARVEL domain-containing proteins and located on human chromosome 10q24.2. MARVELD1 has no significant similarity with other members of MARVEL domain family at amino acid level.