TIMP-3 expression associates with malignant behaviors and predicts favorable survival in HCC.

The tissue inhibitors of metalloproteinases (TIMPs) are proteins that specifically inhibit the proteolytic activity of the matrix metalloproteinases (MMPs). TIMP-3, the only member of the TIMPs that can tightly bind to the extracellular matrix, has been identified as a unique tumor suppressor that demonstrates the ability to inhibit tumor angiogenesis, invasion, and metastasis. This study aimed to detect the expression of TIMP-3 in hepatocellular carcinoma (HCC) and investigate the association between TIMP-3 expression and its clinicopathological significance in HCC patients.

Suppressive effects of simvastatin on the human acute promyelocytic leukemia NB4 cell line through the regulation of the nuclear factor-κB signaling pathway.

The present study examined the effects of simvastatin on the proliferation, apoptosis and gene expression levels involved in the nuclear factor-κB (NF-κB) signaling pathway in the human acute promyelocytic leukemia NB4 cell line by methyl thiazolyl tetrazolium assay, flow cytometry and the Human NF-κB Signaling Pathway RT Profiler™ PCR Array profiles. The results showed that simvastatin significantly inhibited proliferation and induced apoptosis of the NB4 cells in a time- and dose-dependent manner. Changes were noted in the expression levels of 56 genes involved in the NF-κB signaling pathways in the NB4 cells treated with 15 μm simvastatin at 48 h post-incubation, among which, 47 genes were downregulated and 9 were upregulated.

MiR-15b targets cyclin D1 to regulate proliferation and apoptosis in glioma cells.

Aim: To investigate the role and mechanism of miR-15b in the proliferation and apoptosis of glioma.

Methods: The miR-15b mimics were transfected into human glioma cells to upregulate the miR-15b expression. Cyclin D1 was determined by both western blotting analysis and luciferase reporter assay.

Downregulation of ABCG2 protein inhibits migration and invasion in U251 glioma stem cells.

ABCG2 is a member of the ATP-binding cassette transporter family, which has been detected in a wide variety of human aggressive tumors, including glioma stem cells (GSCs), glioma tissues of higher grades, and implanted glioma xenografts. Previous research has implied that ABCG2 might be associated closely with invasion and spread in tumors. However, the specific roles and mechanisms of ABCG2 in regulating the migration and invasion of GSCs remain unclear.

miR-145 inhibits migration and invasion of glioma stem cells by targeting ABCG2.

Despite advances in clinical therapies and technologies, the prognosis for patients with malignant glioma is poor. Our previous research demonstrated that glioma stem cells (GSCs) were crucial for glioma malignancy and accelerated tumor migration and invasion. The migration and invasion of malignant glioma cells into the surrounding normal brain tissues cause the poor outcome.

miR-125b inhibitor enhance the chemosensitivity of glioblastoma stem cells to temozolomide by targeting Bak1.

Temozolomide (TMZ) is a promising chemotherapeutic agent for treating glioblastomas. However, resistance develops quickly with a high frequency. Glioblastoma stem cells (GSCs) causing resistance to drug therapy were considered to be one of key factors.

A functional Ser326Cys polymorphism in hOGG1 is associated with noise-induced hearing loss in a Chinese population.

DNA damage to cochlear hair cells caused by 8-oxoguanine (8-oxoG) is essential for the development of noise-induced hearing loss (NIHL). Human 8-oxoG DNA glycosylase1 (hOGG1) is a key enzyme in the base excision repair (BER) pathway that eliminates 8-oxoG. Many epidemiological and functional studies have suggested that the hOGG1 Ser326Cys polymorphism (rs1052133) is associated with many diseases.

Novel electrochemical sensing platform based on magnetic field-induced self-assembly of Fe3O4@Polyaniline nanoparticles for clinical detection of creatinine.

A novel electrochemical sensing platform based on magnetic field-induced self-assembly of Fe3O4@Polyaniline nanoparticles (Fe3O4@PANI NPs) has been for the first time fabricated for the sensitive detection of creatinine in biological fluids. The template molecule, creatinine, was self-assembled on the surface of Fe3O4@PANI NPs together with the functional monomer aniline by the formation of N-H hydrogen bonds. After pre-assembled, through the magnetic-induction of the magnetic glassy carbon electrode (MGCE), the ordered structure of molecularly imprinted polymers (MIPs) were established by the electropolymerization and assembled on the surface of MGCE with the help of magnetic fields by a simple one-step approach.

miR-125b promotes cell proliferation by directly targeting Lin28 in glioblastoma stem cells with low expression levels of miR-125b.

MicroRNAs (miRNAs) are small noncoding RNA molecules that regulate protein expression by cleaving or repressing the translation of target mRNAs. Our previous studies have revealed that miR-125b is a typical overexpressed miRNA in human primary glioblastoma stem cells (GSCs). Here, we report that miR-125b was also found to be significantly underexpressed in three primary GSCs.

High expression of inositol polyphosphate phosphatase-like 1 associates with unfavorable survival in hepatocellular carcinoma.

Inositol polyphosphate phosphatase-like 1 (INPPL1), also known as SH2-containing inositol 5'-phosphatase 2 (SHIP2), has been suggested to act downstream of the PI3K/AKT pathway and play an important function in tumor development and progression. However, the associations between SHIP2 expression and the clinical features to determine its clinicopathologic significance in hepatocellular carcinoma (HCC) have not been investigated. In the present study, one-step quantitative PCR reverse transcription-polymerase chain reaction (qPCR) and immunohistochemistry (IHC) analysis with HCC tissue microarrays (TMA) were employed to evaluate the expression of SHIP2 in HCC.

Elevated expression of SHIP2 correlates with poor prognosis in non-small cell lung cancer.

SH2-containing inositol 5'-phosphatase 2 (SHIP2) is a vital regulator of phosphoinositide pools in metabolic pathways and is considered to downregulate phosphatidylinositol 3'-kinase signaling, which underlies the development of several kinds of human cancers. However, SHIP2 expression in non-small cell lung cancer (NSCLC) and its relationship with the clinical characteristics of NSCLC remain poorly understood. In this study, one-step quantitative reverse transcription-polymerase chain reaction and immunohistochemistry analysis with tissue microarray was used to evaluate SHIP2 expression in NSCLC and to investigate the relationship of this expression to NSCLC prognosis.

Correlation of Epworth Sleepiness Scale with multiple sleep latency test and its diagnostic accuracy in assessing excessive daytime sleepiness in patients with obstructive sleep apnea hypopnea syndrome.

Background: Excessive daytime sleepiness (EDS) is often associated with obstructive sleep apnea hypopnea syndrome (OSAHS) and contributes to a number of comorbidities in these patients. Therefore, early detection of EDS is critical in disease management. We examined the association between Epworth Sleepiness Scale (ESS) and multiple sleep latency test (MSLT) and diagnostic accuracy of ESS in assessing EDS in OSAHS patients.

miR-125b inhibitor may enhance the invasion-prevention activity of temozolomide in glioblastoma stem cells by targeting PIAS3.

Background: Temozolomide, an alkylating agent, is a promising chemotherapeutic agent for treating glioblastoma. Although chemotherapy with temozolomide may restrain tumor growth for some months, invariable tumor recurrence suggests that cancer stem cells maintaining these tumors persist. Previous research has shown that temozolomide can inhibit the proliferation of human glioblastoma stem cells (GSCs); however, no research has focused on the invasion of GSCs, which is an important factor for glioblastoma recurrence.

WITHDRAWN: Errors Regarding the Article "MicroRNA-21 Modulates Chemosensitivity of Breast Cancer Cells to Doxorubicin by Targeting PTEN".

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Inhibition of nephrin activation by c-mip through Csk-Cbp-Fyn axis plays a critical role in Angiotensin II-induced podocyte damage.

It has been demonstrated that nephrin inactivation plays a critical role in Angiotensin II (AngII)-induced podocyte damage both in in vitro and in vivo, but the underlying molecular mechanisms are still unclear. Recently, c-maf inducing protein (c-mip) has been identified as a key component in the molecular pathogenesis of acquired podocyte diseases. In this study, the role of c-mip on AngII-induced nephrin inactivation and podocyte damage was explored in a mouse podocyte cell line.

miR-335 promotes cell proliferation by directly targeting Rb1 in meningiomas.

Meningiomas, one of the most common benign brain tumors in humans, arise from arachnoid cells in the brain meninges. Our investigations have revealed that miR-335 is a typical microRNA overexpressed in meningiomas in humans. Characterization of the effects of miR-335 overexpression in meningiomas demonstrated that elevated levels of miR-335 increased cell growth and inhibited cell cycle arrest in the G0/G1 phase in vitro; in addition, reduction of the miR-335 levels had the opposite effect on tumor growth and progression.

Functional differences of miR-125b on the invasion of primary glioblastoma CD133-negative cells and CD133-positive cells.

MicroRNAs (miRNAs) are small noncoding RNAs whose function as modulators of gene expression is crucial for the proper control of cell development, differentiation, and homeostasis. The total number and composition of miRNAs expressed per cell at different stages of development varies widely, and the same miRNA may function differently at different stages of development. In this prospective study, we evaluated the function of miR-125b at different developmental stages of glioblastoma cells, such as primary glioblastoma cells and the corresponding stem cells.

MicroRNA-21 inhibitor sensitizes human glioblastoma U251 stem cells to chemotherapeutic drug temozolomide.

MicroRNAs (miRNAs) are small noncoding RNA molecules that regulate protein expression by cleaving or repressing the translation of target mRNAs. In mammals, their function mainly represses the target mRNA transcripts via imperfect complementary sequences in the 3'UTR of target mRNAs. Several miRNAs have been recently reported to be involved in modulation of glioma development, especially some upregulated miRNAs, such as microRNA-21 (miR-21), which has been found to function as an oncogene in cultured glioblastoma multiforme cells.

Quinacrine Inhibits Cell Growth and Induces Apoptosis in Human Gastric Cancer Cell Line SGC-7901.

Background: Quinacrine (QC), an antimalarial drug, has been shown to possess anticancer effect both in vitro (cancer cell lines) and in vivo (mouse models). In the cancer cells, QC can simultaneously suppress nuclear factor-κB and activate p53 signaling, which results in the induction of the apoptosis in these cells. However, the experimental results come from a few limited cancer cell lines, and the detailed mechanisms remain unknown.

Gossypin induces G2/M arrest in human malignant glioma U251 cells by the activation of Chk1/Cdc25C pathway.

Gossypin is a flavone that was originally isolated from Hibiscus vitifolius and has traditionally been used for the treatment of diabetes, jaundice, and inflammation. Recently, gossypin was found to have potent anticancer properties; however, its effect on human gliomas still remain unknown. To investigate the potential anticancer effects of gossypin on malignant gliomas and analyze the associated molecular mechanisms, we treated human glioma U251 cells with gossypin.

MicroRNA-125b-2 confers human glioblastoma stem cells resistance to temozolomide through the mitochondrial pathway of apoptosis.

MicroRNAs (miRNAs) are small, non-coding RNA molecules that regulate protein expression by cleaving or repressing the translation of target mRNAs. miR-125b, one of the neuronal miRNAs, was recently found to be necessary for stem cell fission and for making stem cells insensitive to chemotherapy signals. Temozolomide (TMZ) is a promising chemotherapeutic agent for treating glioblastomas.

[Research on the effects of PIAS3 expression on the invasion of glioma TJ905 cells].

Objectives: To investigate the function and possible mechanisms of PIAS3 expression on the invasion of TJ905 cells.

Methods: PIAS3 overexpression vectors were constructed and PIAS3 siRNA were chemically synthesized, which were separately transfected into TJ905 cells for upregulation or downregulation of PIAS3 expression levels in TJ905 cells. After that, the invasive effects of TJ905 cells were measured by Transwell assay, and the expression of PIAS3, tissue inhibitor of metalloproteinases (TIMP)3, matrix metalloprotease (MMP)-2, and MMP-9 were identified by Western blot.

[Determination of circulating HBV specific CD8+ T cells in hepatitis B patients by flow cytometry and its clinical significance].

Objective: To explore the levels of circulating HBV specific CD8+ T cells in hepatitis B patients and analysis its clinical significance.

Methods: HBV specific CD8+ T cells in whole blood samples of twenty-five acute hepatitis B patients, thirty-five chronic hepatitis B patients and ten healthy control were stained with pentamers complex of HLA-A2 and HBV core 18-27 peptide and counted by flow cytometry.

Results: The medians of HBV core 18-27 specific CD8+ T cells quantities among total CD8+ cells were 2.

[The expression and significance of RKIP in lung squamous cell carcinoma tissues].

Background And Objective: Raf kinase inhibitory protein (RKIP) belongs to the phosphatidylethanolamine binding protein (PEBP) family. RKIP is an endogenous inhibitor of the Raf-1-MEK1/2-ERK1/2 signaling pathway, NFkappaB signaling pathway and G protein coupled receptors signaling pathway. The aim of this study is to explore the expression of RKIP in lung squamous cell carcinoma, and the relationship between RKIP expression and clinical pathology of lung squamous cell carcinoma.

TGF-β1 induces podocyte injury through Smad3-ERK-NF-κB pathway and Fyn-dependent TRPC6 phosphorylation.

TGF-β1 plays an important role on podocyte injury and glomerular diseases, while the underlying molecular mechanisms are still elusive. Here, the potential role of the ion channel TRPC6 and the proximal signaling was explored in TGF-β1-treated mouse podocyte. Our results showed that TGF-β1 significantly increased podocyte apoptosis and induced obvious disorganization of actin filaments in a time-dependent pattern.