The METTL3-mA-YTHDC1-AMIGO2 axis contributes to cell proliferation and migration in esophageal squamous cell carcinoma.

The upregulation of methyltransferase-like 3 (METTL3) has been associated with the progression of esophageal cancer. However, METTL3-induced N-methyladenosine (mA) alterations on the downstream target mRNAs in esophageal squamous cell carcinoma (ESCC) are not yet fully understood. Our study revealed that silencing METTL3 resulted in a significant decrease in ESCC cell proliferation and metastasis in vitro and in vivo.

Ferroptosis involves in Schwann cell death in diabetic peripheral neuropathy.

Accumulating evidence shows that Schwann cells' (SCs) death caused by high glucose (HG) is involved in the pathological process of diabetic peripheral neuropathy (DPN). Ferroptosis is a novel form of regulatory cell death driven by iron-dependent lipid peroxidation. However, it is not clear whether ferroptosis is involved in the death process of SCs induced by HG.

Apigenin regulates the migration, invasion, and autophagy of hepatocellular carcinoma cells by downregulating YAP.

Apigenin is an edible flavonoid with anticancer properties; however, the underlying mechanisms in hepatocellular carcinoma (HCC) remain to be clarified. In the present study, we demonstrated that apigenin decreased the viability of both SMMC-7721 and SK-Hep1 cells in a dose-dependent manner, and inhibited the migration and invasion of HCC cells with different metastatic potential by regulating actin cytoskeletal rearrangements. Moreover, we showed that apigenin decreased the expression of YAP, and subsequently reduced migration and invasion by modulating the expression of the epithelial-mesenchymal transition (EMT) markers, and promoted the autophagy of HCC cells by regulating the expression of autophagy-related genes.

Emerin knockdown induces the migration and invasion of hepatocellular carcinoma cells by up-regulating the cytoplasmic p21.

Emerin (EMD) plays diverse roles in cellular polarity organization, nuclear stability, and cell motility, however, the biological role of EMD relevant to the migration and invasion of hepatocellular carcinoma (HCC) cells has not yet been illustrated. In the present study, we initially found that the upregulation of EMD in HCC tissues, and EMD expression was negatively correlated with the spontaneous metastatic potential of HCC cell lines. Loss of EMD in HCC cells facilitated cell migration and invasion in vitro and metastasis in vivo.

Calmodulin activation of polo-like kinase 1 is required during mitotic entry.

Polo-like kinase 1 (Plk1) is a conserved key regulator of the G2/M transition, but its upstream spatiotemporal regulators remain unknown. With the help of immunofluorescence, co-immunoprecipitation, and glutathione S-transferase (GST) pull-down assay, we found that calmodulin (CaM) is one such regulatory molecule that associates with Plk1 from G2 to metaphase. More importantly, this interaction results in considerable stimulation of Plk1 kinase activity leading to hyperphosphorylation of Cdc25C.

Growth-inhibitory effects of MOB2 on human hepatic carcinoma cell line SMMC-7721.

Aim: To investigate the growth-inhibiting and apoptosis-inducing effects of the gene MOB2 on human hepatic carcinoma cell line SMMC-7721.

Methods: The full-length cDNA of the MOB2 gene was amplified from human umbilical vein endothelial cells. The correct full-length MOB2 cDNA was subcloned into the eukaryotic expression vector pEGFP-C1.

[Effect of genistein on MAPK signal pathway in the collagen-induced arthritis fibroblast-like synoviocytes].

Objective: To study the effect of genistein (Gen) on MAPK signal pathway in the CIA rat fibroblast-like synoviocytes (FLS).

Methods: The rat model of collagen-induced arthritis (CIA) was established. The cultured FLS of CIA rats were divided using randomized method.

Synergistic antitumor effects of in vivo production of human endostatin and tissue inhibitor of metalloproteinase-1 in mice after subcutaneous implantation of primary fibroblasts transfected by adenovirus-mediated gene delivery.

Background: Tissue inhibitor of metalloproteinase (TIMP)-1 is a multifunctional protein. The aim of the study was to examine the feasibility of using a combination of adenovirus-mediated gene delivery of TIMP-1 plus endostatin and cell transplantation techniques to treat tumor growth and metastasis in mouse melanoma.

Methods: A enzyme-linked immunosorbent assay (ELISA) was used to detect the level of TIMP-1 and endostatin in vitro and in vivo.

[Inhibitory effect of genistein on hypoxia-inducible factor-1alpha expression induced by cobalt chloride in leukemia cell line K562].

This study was aimed to investigate the effect of genistein (gen) on the expression of hypoxia inducible factor-1alpha (HIF-1alpha) induced by cobalt chloride (CoCl(2)) in human leukemia cell line K562. The hypoxia condition was simulated by CoCl(2); the dose- and time-effect groups were prepared as follows: the former were exposed to 0, 50, 100 and 150 micromol/L of CoCl(2) for 72 hours, the latter were detected at 0, 24, 48 and 72 hours while treated with CoCl(2) 100 micromol/L. The gen-treated samples were divided into five groups: (1) normal control; (2) CoCl(2) 150 micromol/L; (3) CoCl(2) 150 micromol/L + gen 50 micromol/L; (4) CoCl(2) 150 micromol/L + gen 100 micromol/L; (5) CoCl(2) 150 micromol/L + gen 200 micromol/L.

[Effects of arsenic trioxide on expressions of vascular endothelial growth factor and P-glycoprotein in multidrug resistant leukemia cell line K562/A02].

Objective: To investigate the effects of arsenic trioxide (ATO) on the expressions of vascular endothelial growth factor (VEGF) and P-glycoprotein (P-gp) in K562/A02 cells and to explore the correlation between VEGF and P-gp.

Methods: The inhibition rate of K562/A02 cell proliferation was detected by using methyl thiazolyl tetrazolium assay (MTT); the level of VEGF was detected by enzyme-linked immunosorbent assay (ELISA) and the expression rate of P-gp was determined by flow cytometry (FCM).

Results: 0.

[Effect of arsenic trioxide on VEGF/R and MMP-2, 9 expressed in K562 cells].

Objective: To explore the effect of arsenic trioxide (As2 O3) on the level of VEGF, VEGFR and the activity of MMP-2, 9 in K562 cells.

Methods: The inhibition ratio of K562 cell was detected by MTT assay, the level of VEGF by Enzyme-linked immunosorbent assay (ELISA), the expression ratio of VEGFR by flow cytometry (FCM), and the activity of MMP-2, 9 by gelatin zymography assay.

Results: (1) The IC50 of K562 cells was (2.

Melanoma-associated antigen family protein-D1 regulation of tumor cell migration, adhesion to endothelium, and actin structures reorganization in response to hypoxic stress.

Melanoma-associated antigen family protein-D1 (MAGE-D1) is a recently identified p75 neurotrophin receptor intracellular binding protein and functions as an adaptor that mediates multiple signaling pathways, including Dlx/Msx-mediated transcription. Here, a new regulatory function for MAGE-D1 in tumor cell motility and adhesion to endothelium is described. MAGE-D1 over-expression suppressed HeLa cell and BEL7402 cell migration, invasion, and adhesion to the monolayer of ECV304 cells.

Inhibition of adenovirus-mediated human MAGE-D1 on angiogenesis in vitro and in vivo.

MAGE-D1 is a member of the MAGE family of proteins, and functions as an adaptor that mediates multiple signaling pathways. The current study for the first time provides evidence for a role of MAGE-D1 in the negative regulation of angiogenic activity in vitro and in vivo models. Our findings showed that MAGE-D1 over-expression significantly suppressed the angiogenic key events such as endothelial cell migration and invasion, adhesion on collagen I substrate, and in vitro differentiation into tube-like structures under both normoxic and hypoxic conditions.

Calmodulin is essential for angiogenesis in response to hypoxic stress in endothelial cells.

Angiogenesis, the formation of new blood vessels that is regulated by hypoxia, is a critical process for the growth and spread of tumors. Multiple phases of this process, including migration, adhesion, and formation of new capillary tubes, are needed for optimal tumor growth. Here, a new regulatory function for Ca2+-CaM in the vascular endothelium is described.

[Inhibitory effects of Scutellaria barbatae D. Don on tumor angiogenesis and its mechanism].

Background & Objective: Various chemically synthetic anti-angiogenesis agents have serious side effects. The traditional Chinese medicine has attracted considerable attention because of its low toxicity. This study was to explore the inhibitory effects of Scutellaria barbatae D.

Knockdown of c-Met by adenovirus-delivered small interfering RNA inhibits hepatocellular carcinoma growth in vitro and in vivo.

c-Met is highly expressed and constitutively activated in various human tumors. We employed adenovirus-mediated RNA interference technique to knock down c-Met expression in hepatocellular carcinoma cells and observed its effects on hepatocellular carcinoma cell growth in vitro and in vivo. Among the five hepatocellular carcinoma and one normal human liver cell lines we analyzed, c-Met was highly expressed and constitutively tyrosine phosphorylated in only MHCC97-L and HCCLM3 hepatocellular carcinoma cells.

RNA interference and its current application in mammals.

Objective: The aim of this review was to assess RNA interference (RNAi) and its possibility as a potential and powerful tool to develop highly specific double-stranded RNA (dsRNA) or small interfering RNA (siRNA) based gene-silencing therapeutics.

Data Sources: The data used in this review were obtained from the current RNAi-related research reports.

Study Selection: dsRNA-mediated RNAi has recently emerged as a powerful reverse genetic tool to silence gene expression in multiple organisms.