Analysis of the mRNA export protein ZC3H11A in HCMV infection and pan-cancer.

Background: We have previously reported that human cytomegalovirus (HCMV) infection could promote the progression of glioma. Here we discovered a stress-induced nuclear protein ZC3H11A (ZC3) through high-throughput sequencing after HCMV infection, which has been reported recently by our research group in regulating mRNA export under stress conditions. And also, a thorough analysis of ZC3 in pan-cancer and the omics data of ZC3 are yet to be conducted.

Human Cytomegalovirus Infection Activates Glioma Activating Transcription Factor 5 via microRNA in a Stress-Induced Manner.

Human cytomegalovirus (HCMV) harnesses a cell-specific manner to infect human nervous system cancer cells, establishes a life-long persistent infection without cell death, and modulates signaling pathways associated with cancer. We previously identified that the HCMV immediate-early 2 (IE2-86) protein binds and activates activating transcription factor 5 (ATF5), a survival factor in many tumor cells. In this study, we investigated a new mechanism of stress-induced miRNA regulation at the ATF5 3' UTR under the HCMV infection and other cellular stress conditions.

Erratum: Construction of the plasmid for expression of EGFP-M-IL-2(88Arg, 125Ala) fusion protein and the anti-tumor effects exerted by the fusion protein in HeLa-60 cells.

[This corrects the article DOI: 10.3892/ol.2015.

Revisiting the phosphotyrosine binding pocket of Fyn SH2 domain led to the identification of novel SH2 superbinders.

Protein engineering through directed evolution is an effective way to obtain proteins with novel functions with the potential applications as tools for diagnosis or therapeutics. Many natural proteins have undergone directed evolution in vitro in the test tubes in the laboratories worldwide, resulting in the numerous protein variants with novel or enhanced functions. we constructed here an SH2 variant library by randomizing 8 variable residues in its phosphotyrosine (pTyr) binding pocket.

Human cytomegalovirus infection enhances invasiveness and migration of glioblastoma cells by epithelial-to-mesenchymal transition.

Objective: This study aims to investigate the effect of human cytomegalovirus (HCMV) infection on epithelial-to-mesenchymal transition (EMT) in glioblastoma cells and the possible underlying molecular mechanism.

Methods: We established primary cell cultures and measured the expression of the HCMV immediate early protein (IE1) to determine HCMV infection by immunohistochemical assays. Human glioma cells were divided into four groups: primary HCMV-positive, primary HCMV-negative, HCMV-positive U87, and HCMV-negative U87 cells.

IE86 Inhibits the apoptosis and promotes the cell proliferation of glioma cells via the hnRNP A2/B1-mediated alternative splicing of Bcl-x.

Human cytomegalovirus (HCMV), a ubiquitous pathogen, can cause severe illness in immunocompromised individuals. Typically, glioma is one of the most common malignant primary brain tumors and originates in the central nervous system. The IE86 gene of HCMV exerts a major role in regulating virus replication.

HCMV-encoded IE2 induces anxiety-depression and cognitive impairment in UL122 genetically-modified mice.

Although there is a high risk of mood disorders and cognitive impairment in congenital human cytomegalovirus (HCMV) infections, the molecular pathogenetic mechanisms of HCMV have not yet been fully determined. In this study, we show that immediate-early 2 (IE2) protein modulates affective and cognitive behaviors. We used a UL122 genetically-modified mice model that can continuously express IE2 protein.

Human cytomegalovirus ie2 affects the migration of glioblastoma by mediating the different splicing patterns of RON through hnRNP A2B1.

Glioblastoma is the most aggressive intracranial tumor and diffuse migration is the leading cause of death. Recent evidence has indicated that heterogeneous nuclear ribonucleoprotein A2B1 (hnRNP A2B1) is overexpressed in human glioblastoma tissue and enhances glioblastoma invasion in vitro. We found by mass spectrometry that hnRNP A2B1 interacts with human cytomegalovirus (HCMV) immediate early 86 protein (IE86, ie2 gene-encoded) in malignant glioma cells (U87MG) infected with HCMV.

The Inhibition of miR-144-3p on Cell Proliferation and Metastasis by Targeting TOP2A in HCMV-Positive Glioblastoma Cells.

Glioblastoma (GBM), the most common type of primary tumor in the central nervous system, is a very aggressive brain tumor with poor prognosis and a high recurrence rate. Increasing evidence suggests that human cytomegalovirus (HCMV) infection is related to GBM and leads to GBM cell growth and metastasis. MicroRNAs are important regulators in the growth and metastasis of glioblastoma.

TLR3 regulates PD-L1 expression in human cytomegalovirus infected glioblastoma.

Glioblastoma, the most common primary brain tumor of adults, is characterized by poor survival rates. Programmed death ligand 1 (PD-L1, CD274) has been implicated in the immune escape of glioblastoma. The presence of human cytomegalovirus (HCMV) in glioblastoma multiforme (GBM) has sparked considerable interest and controversy.

HCMV-encoded IE2 promotes NAFLD progression by up-regulation of SREBP1c expression in UL122 genetically modified mice.

Non-alcoholic fatty liver disease (NAFLD), a liver manifestation of metabolic syndrome, is associated with considerable health and socioeconomic burdens in many populations worldwide. Recent studies suggest that human cytomegalovirus (HCMV) infection might play a role in the pathogenesis of metabolic diseases, including NAFLD, but it is still unclear whether HCMV-encoded IE2 plays an important role in this process. Interestingly, SREBP1c was recently reported to play critical roles in the development of hepatic steatosis.

Over-expression of TOP2A as a prognostic biomarker in patients with glioma.

Topoisomerase (DNA) II alpha (TOP2A), an enzyme that controls and alters the topologic states of DNA during transcription, is aberrantly expressed in many cancers. However, few studies have investigated expression of TOP2A and its clinical significance in glioma. We retrieved six independent investigations from the Oncomine database and found that TOP2A is highly expressed in glioma tissues compared with corresponding normal controls.

SUMO2/3 modification of activating transcription factor 5 (ATF5) controls its dynamic translocation at the centrosome.

Activating transcription factor 5 (ATF5) is a member of the ATF/cAMP response element-binding protein family of transcription factors. ATF5 regulates stress responses and cell survival, proliferation, and differentiation and also plays a role in viral infections, cancer, diabetes, schizophrenia, and the olfactory system. Moreover, it was found to also have a critical cell cycle-dependent structural function at the centrosome.

Cx43 and NMDA receptors changes in UL122 genetically modified mice hippocampus: a mechanism for spatial memory impairment.

Congenital HCMV infection has been reported to be involved in learning and memory impairment, but whether HCMV IE2 plays a key role in the process remains unknown. The purpose of this study was to study the effects of IE2 on the expression levels of NMDA receptors and CX43 in the hippocampal neurons of ul122 transgenic mice. Firstly, the ul122 genetically modified mice models that can steadily and continuously express IE2 protein were established.

MicroRNA-613 is downregulated in HCMV-positive glioblastoma and inhibits tumour progression by targeting arginase-2.

Glioblastoma is the most common and malignant tumour that occurs primarily in nervous system and has a high morbidity. Research on glioblastoma has recently focused on human cytomegalovirus, belonging to the beta subfamily of Herpesviridae that plays crucial roles in cancer development and progression. This study aimed to investigate the role of human cytomegalovirus-associated microRNA-613 in glioblastoma.

miR-141-3p functions as a tumor suppressor modulating activating transcription factor 5 in glioma.

Glioma is the most common malignant primary brain tumor which arises from the central nervous system. Our studies reported that an anti-apoptotic factor, activating transcription factor 5 (ATF5), is highly expressed in malignant glioma specimens and cell lines. Downregulation by dominant-negetive ATF5 could repress glioma cell proliferation and accelerate apoptosis.

Human cytomegalovirus immediate-early protein promotes survival of glioma cells through interacting and acetylating ATF5.

Human cytomegalovirus (HCMV), a widespread beta-herpes virus, infects a high percentage of gliomas. HCMV is specifically detected in human gliomas at a low level of expression raises the possibility that it may regulate the malignant phenotype in a chronic manner. Although HCMV is not recognized as an oncogenic virus, it might dysregulate signaling pathways involved in initiation and promotion of malignancy.

Human cytomegalovirus infection promotes the stemness of U251 glioma cells.

Glioblastoma (GBM) are the most common and aggressive tumors of human brain. Recent studies showed that human cytomegalovirus (HCMV) can induce malignant transformation of tumor cells to maintain stemness. Transcription factor 5 (ATF5) is an anti-apoptotic protein that is highly expressed in malignant glioma.

Antiviral effects of IFIT1 in human cytomegalovirus-infected fetal astrocytes.

The prominent feature of human cytomegalovirus (HCMV) is cell tropism specificity for human fetal nervous system, which leads to severe fetal nervous system damage especially in first-trimester gestation. In this study, human astrocytes isolated from fetal brain were infected with HCMV AD169 and whole genome transcriptome profile was performed. The results showed that the gene expression of interferon stimulated genes (ISGs), chemokine and chemokine receptors were significantly up-regulated (P < 0.

Association between human cytomegalovirus infection and histone acetylation level in various histological types of glioma.

At present, glioma is the most common intracranial tumor and accounts for 40-60% of intracranial tumors. Glioma is highly anaplastic and demonstrates invasive growth. Although considerable progression has been achieved in the treatment of malignant glioma, the prognosis of this disease remains poor.

DNA methylation level of promoter region of activating transcription factor 5 in glioma.

Transcription factors, which represent an important class of proteins that play key roles in controlling cellular proliferation and cell cycle modulation, are attractive targets for cancer therapy. Previous researches have shown that the expression level of activating transcription factor 5 (ATF5) was frequently increased in glioma and its acetylation level was related to glioma. The purposes of this study were to explore the methylation level of ATF5 in clinical glioma tissues and to explore the effect of ATF5 methylation on the expression of ATF5 in glioma.

Construction of the plasmid coding for the expression of the EGFP--2(Arg, Ala) fusion protein and the anti-tumor effects exerted by the fusion protein in HeLa-60 cells.

Gene therapy is a promising therapeutic option for the treatment of various cancers, and tumor-targeted plasmids encoding toxic protein genes are potential tools for gene therapy. In the present study, a recombinant plasmid containing the genes for the toxic protein melittin and interleukin-2 (IL-2) was constructed. Melittin and IL-2 are known to play key roles in immunoregulation and cancer therapy, but they each possess defects that limit the clinical application of these proteins.

Survivin expression and serum levels in pancreatic cancer.

Background: Survivin, an inhibitor of apoptosis, is overexpressed in pancreatic ductal adenocarcinoma (PDAC). Its expression is known to be associated with poor clinical outcome. However, to our knowledge, there has been no study to characterize its usefulness as a serum marker for human pancreatic cancer.

Upregulation of Toll-like receptor 2 expression in colorectal cancer infected by human cytomegalovirus.

The aim of the present study was to investigate the association between Toll-like receptor 2 (TLR2) expression and human cytomegalovirus (HCMV) in colorectal carcinoma by detecting the expression of IE1-72, TLR2, TLR4 and tumor necrosis factor (TNF)-α in colorectal carcinoma and colon adenoma samples, as well as by analyzing the mRNA levels of the proteins in colon cancer cell lines, following HCMV infection. For this study, 56 colorectal cancer and 36 colon adenoma samples were collected, and normal mucosal tissue adjacent to the tumor was used as the control. The expression of the IE1-72, TLR2, TLR4, nuclear factor (NF)-κB and TNF-α protein was detected by immunohistochemistry.

HCMV induces dysregulation of glutamate uptake and transporter expression in human fetal astrocytes.

Human cytomegalovirus (HCMV) infections are the leading cause of viral induced birth defects, affecting the central nervous system (CNS) primarily. Fetal CNS is especially vulnerable to CMV induced injury. As HCMV permissive cells, astrocytes are responsible for major glutamate transport and regulate extracellular levels of glutamate avoiding its accumulation which is implicated in neurodegenerative disorders.