Molecular Medicine Reports (Mol Med Rep )

Description

  • Impact factor
    1.17
  • 5-year impact
    0.96
  • Cited half-life
    1.90
  • Immediacy index
    0.26
  • Eigenfactor
    0.00
  • Article influence
    0.22
  • Website
    Molecular Medicine Reports website
  • ISSN
    1791-2997
  • OCLC
    248467032
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Parkinson's disease (PD) is one of the most common age‑related neurodegenerative diseases, which results from a number of environmental and inherited factors. PD is characterized by the slow progressive degeneration of dopaminergic (DA) neurons in the substantia nigra. The nigrostriatal DA neurons are particularly vulnerable to inflammatory attack. Neuroinflammation is an important contributor to the pathogenesis of age‑related neurodegenerative disorders, such as PD, and as such anti‑inflammatory agents are becoming a novel therapeutic focus. This review will discuss the current knowledge regarding inflammation and review the roles of intracellular inflammatory signaling pathways, which are specific inflammatory mediators in PD. Finally, possible therapeutic strategies are proposed, which may downregulate inflammatory processes and inhibit the progression of PD.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Tumor metastasis is a prominent cause of treatment failure in cervical carcinoma. Phenethyl isothiocyanate (PEITC) is an active component extracted from cruciferous plants that has exhibited anticancer activity in various types of human cancer; however, its effect on the inhibition of metastasis remains unclear. The current study aimed to explore the effect of PEITC on the suppression of metastasis in HeLa cervical carcinoma cells. Multiple variables were assessed with different methods as follows: Cell viability, with a Vi‑CELL analyzer; cell adhesion, by MTS assay; cell invasion, by Transwell assay; cell cycle, by flow cytometry assay; cytokine concentration, by ELISA assay; metastasis‑related gene and protein expression, by quantitative polymerase chain reaction and western blotting; and transcription factor activity, by gene reporter assay. The results indicated that PEITC exhibited an inhibitory effect on the adhesion and invasion of HeLa cells by induction of G2/M phase arrest, it reduced the expression of CDK1, MMP‑2/9, CD44, ICAM‑1, increased the production of TGF‑β, IL‑6 and IL‑8, and increased the phosphorylation of Smad2. These results suggest that PEITC may be a potential antitumor compound, acting through the TGF‑β/Smad2 pathway; and it has the potential for future use as a therapy for cervical carcinoma subsequent to further studies.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Chromosomal abnormalities and the 22q11 microdeletion are implicated in congenital heart defects (CHDs). This study was designed to detect these abnormalities in fetuses and determine the effect of genetic factors on CHD etiology. Between January 2010 and December 2011, 113 fetuses with CHD treated at the Beijing Obstetrics and Gynecology Hospital were investigated, using chromosome karyotyping of either amniotic fluid cell or umbilical cord blood cell samples. Fetuses with a normal result were then investigated for the 22q11 microdeletion by fluorescence in situ hybridization. Of the 113 patients, 12 (10.6%) exhibited chromosomal abnormalities, while 6 (5.3%) of the remaining 101 cases presented with a 22q11 microdeletion. The incidence of chromosomal abnormalities was significantly higher in the group of fetuses presenting with extracardiac malformations in addition to CHD (P<0.001), although the detection of the 22q11 microdeletion was not significantly different between the two groups (P=0.583). In addition, all fetuses with the 22q11 microdeletion occurred de novo. In conclusion, genetic factors are important in the etiology of CHD. Where fetuses present with cardiac defects, additional chromosomal analysis is required to detect extracardiac abnormalities. Fetuses with heart defects should also be considered for 22q11 microdeletion detection to evaluate fetal prognosis, particularly prior to surgery.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: MicroRNAs (miRs) are small non‑coding RNAs with regulatory roles, which are involved in a broad spectrum of physiological and pathological processes, including cancer development and progression. However, the function of miR‑185 in the development of human colon cancer has not yet been investigated. In this study, the association between miR‑185 expression and the clinicopathological characteristics of patients with colon cancer was analyzed using quantitative polymerase chain reaction (qPCR). Using a gain‑of‑function approach, the effects of miR‑185 overexpression on the expression of hypoxia‑inducible factor‑2α (HIF‑2α), proliferating cell nuclear antigen (PCNA) and matrix metallopeptidase‑2 (MMP‑2) were investigated in SW620 colon cancer cells using qPCR and western blotting. Functional analysis of cellular proliferative activities, by MTT assay, and invasive potential, by Transwell assay, was conducted on SW620 cells expressing low levels of miR‑185. miR‑185 was found to be significantly downregulated in cancer tissues compared with adjacent non‑cancerous tissues, and was negatively correlated with lymph node metastasis of colon cancer (P<0.001). miR‑185 overexpression in vitro impeded cellular proliferation and invasive potential with reduced expression of HIF‑2α, PCNA and MMP‑2 in SW620 cells transfected with an miR‑185 mimic. In addition, the tumor volumes in SW620 subcutaneous nude mouse models treated with miR‑185 were significantly smaller than those of the control group. In conclusion, these findings indicate that miR‑185 as a tumor suppressor may affect the development of colon cancer cells via inhibition of HIF‑2α signaling, suggesting that miR‑185 may serve as a potential therapeutic target in cancer treatment.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Previous studies by our group revealed that the phosphoinositide 3‑kinase (PI3K)/AKT pathway was involved in estrogen‑induced metastasis in ovarian cancer cells. In the present study, the role and mechanism of estrogen‑induced invasion was further explored using a stable short hairpin RNA (shRNA) estrogen receptor α/β (ER α/β) SKOV3 cell line when ER α and ER β were knocked down by lentiviral infection. The effects of estrogen and LY294002, a PI3K inhibitor, on the invasion of shRNA ER α/β SKOV3 cells were evaluated in vitro and in vivo. 17‑β estradiol promoted cell invasion, activated phosphorylated AKT in a dose‑ and time‑dependent manner, decreased E‑cadherin and increased cytoplasmic α‑actinin‑4 expression. When the PI3K/AKT pathway was suppressed by LY294002, the effect of estrogen was attenuated. Estrogen stimulated the growth of shRNA ER α/β SKOV3 xenograft tumors in nude mice, whereas LY294002 inhibited the growth and antagonized the effect of estrogen. The results indicate that estrogen promotes the invasion of ovarian cancer cells via activation of the PI3K/AKT pathway, downregulation of E‑cadherin and upregulation of α‑actinin‑4 in an ER‑independent manner. Inhibiting the PI3K/AKT pathway may be a useful treatment for ovarian carcinoma.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: High levels of homocysteine, caused by abnormal methionine metabolism, can induce degeneration of mouse hippocampal neurons. iTRAQ™ technology has been widely used in the field of proteomics research and through employing this technology, the present study identified that hyperhomocysteinemia induced the downregulation of 52 proteins and upregulation of 44 proteins in the mouse hippocampus. Through gene ontology and pathway analysis, the upregulation of components of the cytoskeleton, actin, regulators of focal adhesion, calcium signaling pathways, tight junctions, ErbB and gonadotrophin‑releasing hormone signaling, leukocyte, transendothelial migration, propanoate and pyruvate metabolism, valine, leucine and isoleucine biosynthesis, synthesis and degradation of ketone bodies and benzoate degradation via CoA ligation pathway, was identified. It was additionally verified that tau protein was highly expressed in the hyperhomocysteinemic neurons. Further analysis revealed that tau network proteins played functional roles in homocysteine‑induced neuronal damage.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Increasing evidence has demonstrated that cell adhesion molecule 1/tumor suppressor in lung cancer 1 (CADM1/TSLC1) is crucially implicated in various biological processes, including proliferation, apoptosis, and invasion during tumorigenesis and development. However, the mechanism underlying its suppression of tumor growth and metastasis in melanoma remains elusive. The aim of the present study was to examine if CADM1/TSLC1 was able to induce growth suppression in melanoma. The plasmid pcDNA3.1‑CADM1/TSLC1 was transfected into A375 cells (a human melanoma cell line). The expression of CADM1/TSLC1 in the transfected cells was determined by RT‑PCR and western blotting analysis. Cell growth was measured by an 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyl‑tetrazolium bromide assay and cell apoptosis was determined by flow cytometry, while a transwell assay was utilized to measure the ability of invasion. The expression of MMP‑2 and MMP‑9 in the transfected cells was determined by western blotting analysis. RT‑PCR and western blotting revealed that in pcDNA3.1‑CADM1/TSLC1 the protein expression of CADM1/TSLC1 protein was higher than in the pcDNA3.1 and A375 cells. The expression of MMP‑2 and MMP‑9 was lower in the pcDNA3.1‑CADM1/TSLC1 than that in the pcDNA3.1 and A375 cells. The growth of CADM1/TSLC1‑transfected cells was significantly suppressed in vitro and the ability of invasion was also reduced, CADM1/TSLC1 was able to induce cell apoptosis. Furthermore, CADM1/TSLC1 was an anti‑invasive gene, the overexpression of which inhibited the invasion of A375 cells. This inhibition may be due to the suppression of the MMP‑2 and MMP‑9 expression, which is relative to tumor metastasis and progression.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Numerous Euphorbiaceae plants have been used for the treatment of diseases, including liver diseases, asthma and rheumatism. The present study evaluated the effect of methanol extracts from Euphorbia cooperi (MEC), a member of the Euphorbiaceae plant family, on the production of inflammatory cytokines interleukin (IL)‑6 and tumor necrosis factor (TNF)‑α, nitric oxide (NO) as well as the activation of mitogen‑activated protein kinase and nuclear factor (NF)‑κB signaling. Non‑cytotoxic concentrations of MEC significantly reduced the production of NO and IL‑6, but not TNF‑α, in lipopolysaccharide (LPS)‑stimulated RAW 264.7 macrophages. The decreased production of NO by MEC was due to alleviated expression of inducible NO synthase. Reporter assays with cells treated with MEC demonstrated reduced activator protein‑1 (AP-1) activity, while NF‑κB activity was not reduced. Furthermore, the phosphorylation levels of c‑Jun N‑terminal kinase (JNK) and p38 were suppressed by MEC while phosphorylation levels of inhibitor of κB were not reduced by MEC, suggesting that MEC‑mediated inactivation of JNK and p38 is the underlying regulatory mechanism for inflammatory mediators in LPS‑stimulated RAW 264.7 macrophages.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Pancreatic cancer has the poorest prognosis among all cancer types, due to its late diagnosis and the lack of effective therapies. Therefore, identification of novel gene targets, which are differentially expressed in pancreatic cancer and functionally involved in the malignant phenotype, is critical to achieve early diagnosis and develop effective therapeutic strategies. microRNAs (miRNAs) are small non-coding RNAs, which negatively regulate the expression of their targets. Due to their various targets, miRNAs play a key role in a number of physiological processes and in oncogenesis. Therefore, investigating the role of miRNAs in tumor may contribute to the development of new diagnostic and therapeutic tools for various types of cancer, including pancreatic cancer. Here, we investigated the role of miR-193b in pancreatic cancer. Our data showed that the expression of miR-193b is markedly decreased in pancreatic cancer tissues compared to adjacent healthy tissues. The Panc-1 cell line transfected with the miR‑193b exhibited significantly decreased proliferative, migratory, and invasive ability compared to untransfected cells. Moreover, miR-193b inhibited the expression of stathmin 1 (STMN1) and urokinase-type plasminogen activator (uPA) in Panc-1 cells. These data suggest that miR-193b acts as a tumor suppressor in pancreatic cancer. Therefore, miR-193b may constitute a promising therapeutic agent for the suppression of pancreatic cancer cell growth and metastasis.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: The period circadian clock 2 (per2) gene plays an important role in modulating the circadian rhythm in the central nervous system. Its protein product, PER2, is mainly expressed in the suprachiasmatic nucleus (SCN) and limbic system, including the central nucleus of the amygdala (CeA), the bed nucleus of the stria terminalis (BNST) and the hippocampus. PER2 rhythmic expression regulates hypothalamus‑pituitary‑adrenal (HPA) axis excitability and circadian rhythm via integration of optical signals and corticotropin‑releasing factor (CRF) stress‑related neurotransmitters, resulting in circadian rhythmicity in target organs. Moreover, glucocorticoids and glucocorticoid receptors exert strong negative feedback to the HPA axis and certain regions of the limbic system, modulating rhythmic per2 expression in peripheral organs. To date, the mechanism of action of PER2 in the limbic system and the HPA axis remains unclear, yet the per2 gene is considered valuable in clinical research for the study of metabolic syndromes, functional gastrointestinal disorders and certain liver diseases. In this review, we summarize the biological effects of the per2 gene and its protein product, PER2, in the limbic system, its involvement in regulation of the HPA axis by the limbic system and the resulting effects on the biological rhythm of target organs, and its clinical significance.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Accumulating evidence has implicated that liraglutide, one of the human glucagon‑like peptide‑1 (GLP‑1) analogues, elicits protective effects on diabetic nephropathy; however, the mechanism has yet to be fully elucidated. The present study aimed to assess the effect and underlying mechanisms of liraglutide in diabetic nephropathy. Wistar rats with streptozotocin‑induced diabetes mellitus were subcutaneously injected with liraglutide or phosphate buffer for 12 weeks at a dose of 0.3 mg/kg/12 h. The biochemical parameters were determined, renal histological examination was performed by hematoxylin and eosin and periodic acid Schiff base staining, and the mRNA levels of nuclear factor κB (NF‑κB) and endothelial nitric oxide synthase (eNOS) were assessed by quantitative polymerase chain reaction. Furthermore, the protein expression of NF‑κB and eNOS as well as eNOS phosphorylation were examined by western blot analysis and the levels of inflammatory cytokines downstream of NF‑κB were evaluated by fluorescence-assisted cell sorting and finally, the eNOS activity and nitric oxide (NO) production were evaluated by ELISA. Liraglutide decreased the levels of total cholesterol, urine, 24-h urinary albumin, blood urea nitrogen, serum creatinine and histological damage. Liraglutide also reduced the expression of NF‑κB at mRNA and protein levels; the expression of tumor necrosis factor‑α, interferon‑γ, interleukin‑6 and monocyte chemoattractant protein‑1 were also reduced. By contrast, eNOS phosphorylation, eNOS activity and NO production appeared to have increased. Liraglutide may have a direct beneficial effect on diabetic nephropathy by improving eNOS activity by inhibiting the NF‑κB pathway without eliciting a glucose lowering effect.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Piperine is an important active component of the Chinese herb Large leaf moss. The aim of this study was to investigate the effects of piperine on oxidative stress. An oxidative stress model was developed in rabbit atrial cells treated with low concentrations of hydrogen peroxide (H2O2). A primary cell culture of the atrial cells was established and the cells were randomly divided into three groups: A piperine group, an H2O2 group and a control group. The results demonstrated that the cell viability and superoxide dismutase activity in the piperine group were significantly higher than in the H2O2 group (P<0.05), and the expression levels of malondialdehyde and glutathione were significantly reduced in the piperine group compared with the H2O2 group (P<0.05). The intracellular free calcium concentration and the expression level of mitochondrial mRNA in the piperine group were also significantly lower than in the H2O2 group (P<0.05). In conclusion, piperine was important in protecting the primary rabbit atrial cells from oxidative stress.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Peroxisome proliferator‑activated receptor γ (PPARγ) may play an important role in lipid metabolism directly or by inducing the transcription of target genes. The aim of the present study was to investigate the association between common variants at the PPARγ locus (C1431T and Pro12Ala polymorphisms) and lipid serum levels. The studied population consisted of 820 subjects randomly selected from the Prevention of Multiple Metabolic Disorders and Metabolic Syndrome in Jiangsu Province cohort population. All subjects were interviewed and blood samples were obtained for laboratory analysis and DNA extraction. The TaqMan single nucleotide polymorphism genotyping assay was used for polymorphism genotyping. Individual polymorphisms and haplotype data were available for analysis. The 12Ala allele was found to be associated with significantly increased levels of triglyceride (TG) (P<0.01), whilst the 1431T allele was found to be associated with significantly increased levels of TG, total cholesterol (TC) and non‑high‑density lipoprotein (non‑HDL) (P<0.01). When P‑C, the most common haplotype, was used as the reference group, the P‑T, A‑C and A‑T haplotypes were found to be associated with significantly increased levels of TG (P<0.01). In addition, the A‑T haplotype was shown to be associated with significantly increased levels of TC and non‑HDL (P<0.01). In conclusion these results suggest that PPARγ gene variability may increase the risk of dyslipidemia.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Cerebellar glioblastomas (GBMs) are rare, with neither their pathogenesis nor prognosis being completely understood. The present study aimed to clarify the clinical characteristics of cerebellar GBMs by comparison with supratentorial GBMs, focusing particularly on the pathogenesis. The clinical factors between cerebellar (n=10) and supratentorial (n=216) GBMs were compared. Additionally, p53 and epidermal growth factor receptor (EGFR) levels were investigated in six patients by immunostaining as well as the isocitrate dehydrogenase 1 (IDH1) status of five patients by direct sequencing. Eight males and two females participated in the present study, the mean age at diagnosis was 56.6 years and the range 37-75 years. Four patients presented with hydrocephalus and one with brainstem involvement, and two patients were diagnosed with neurofibromatosis type 1. Two patients had previously received radiotherapy, eight patients received postoperative radiotherapy and seven chemotherapy. The mean Karnofsky performance status (KPS) score was lower in patients with cerebellar GBMs compared to those with supratentorial GBM; however, the survival times did not differ between the two groups. All of the cases of six cerebellar GBMs were p53‑positive and EGFR‑negative, as detected by immunostaining, consistent with secondary GBM. However, no IDH1 mutations were detected in any of the five cases of cerebellar GBMs analyzed, indicating that these tumors were not of the secondary type. The KPS score with cerebellar GBMs may be lower due to hydrocephalus, which was ameliorated by surgery but may have impacted the survival rate. It was confirmed that cerebellar GBMs were identical to supratentorial GBMs with respect to its clinical features, with the possible exception of the KPS score. The present study's genetic analyses indicated that cerebellar GBMs may develop via a pathway different from that of either primary or secondary GBM.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Hepatocellular carcinoma (HCC) accounts for the majority of liver cancers. A hypoxic microenvironment is a common feature of HCC, and is associated with malignant invasion, metastasis and epithelial-mesenchymal transition (EMT) changes. Curcumin is a botanical agent derived from the dried rhizome of Curcuma longa. Although a number of preclinical studies have shown that curcumin has anticancer properties when administered in a normoxic microenvironment, no studies have directly examined the effect of curcumin on preventing HCC invasion and metastasis under hypoxic conditions. This study aimed to determine whether curcumin has effects on the hypoxia-induced malignant biological behavior of HCC. CoCl2 was used to establish a hypoxia model in vitro. The results showed that curcumin significantly decreased hypoxia-induced hypoxia inducible factor-1α (HIF-1α) protein level in HepG2 cells. Furthermore, cell proliferation, migration and invasiveness, as well as EMT changes associated with HIF-1α accumulation generated by a hypoxic microenvironment, were eliminated by curcumin. In conclusion, these data indicate that curcumin may be a viable anticancer agent in the treatment of HCC.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Aminopeptidase N (APN) is important in tumour processes. The present study detected the anti‑tumour activity of the novel APN inhibitor DH‑12a, which is an indoline‑2,3‑dione derivative. In the present study, Bestatin, a clinical APN inhibitor was used as a positive control. The expression of APN in the ES-2 and 3AO cell lines were assessed using flow cytometry and the drug inhibition constants of DH‑12a (Ki=13.15 µM) and Bestatin (Ki=16.57 µM) were assessed using a double reciprocal method of competitive inhibition. The in vitro effects of DH‑12a on cell proliferation were assessed using a 3‑(4,5‑dimethyl‑thiazol‑2‑yl)‑2,5‑diphenyl tetrazolium bromide assay on human cell lines of ES‑2 (IC50=43.8 µM), A549 (inhibition rate=41.5% at 160 µM DH‑12a), HL60 (inhibition rate=47.83% at 160 µM DH‑12a) and 3AO (IC50=70.2 µM). The inhibition rates were consistently higher than those of Bestatin. The effects of DH‑12a on cell migration (inhibition rates in ES‑2 cells and 3AO cells were 56.4 and 76.5%, respectively at 15 µM) and invasion (inhibition rates in ES‑2 cells and 3AO cells were 75.6 and 66.5%, respectively at 15 µM) were assessed using transwell plates. The in vivo effects of DH‑12a on tumour proliferation and lung tumour metastasis were determined using an H22 xenograft mice model, where DH‑12a was administered in combination with genotoxic 5‑fluorouracil. The anti‑tumour activities of DH‑12a in vivo were also greater than those of Bestatin. In conclusion, the in vitro effects of DH‑12a on tumour proliferation, migration and invasion were consistent with the in vivo effects. In addition, DH‑12a exhibited greater anti‑tumour properties compared with Bestatin.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Oxaliplatin and the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA), also known as vorinostat, are potent antitumor agents. The aim of this study was to investigate the effect of SAHA on the antitumor efficacy of oxaliplatin in gastric cancer and the interaction between oxaliplatin and SAHA. Cell growth inhibition was evaluated using Cell Counting Kit‑8 and colony formation assays. Xenografts established in nude mice were used to assess tumor growth in vivo. Western blot analysis was used to detect the expression of acetyl‑histone H3, phosphorylated histone H2AX (γH2AX), B‑cell lymphoma 2 (Bcl‑2), cleaved caspase‑3, cleaved poly (ADP‑ribose) polymerase (PARP), phosphorylated- (p-)Src, Src, Akt and p‑Akt in gastric cancer cells. The in vitro growth of SGC‑7901, Hs746T and MKN28 gastric cancer cells was found to be dose‑dependently inhibited by oxaliplatin and SAHA. Furthermore, combined treatment was observed to be more effective in inhibiting cancer cell growth and colony formation than monotherapy. Similar effects were found in the xenografts. A positive interaction was identified between oxaliplatin and SAHA (between‑subject effects of oxaliplatin and SAHA, P<0.001). In addition, combined exposure to oxaliplatin and SAHA increased γH2AX expression and decreased Bcl‑2 expression. The expression of cleaved caspase‑3 and PARP was also increased with combination treatment. Oxaliplatin‑induced Src phosphorylation was detected in gastric cancer cells, as we have previously reported. However, this effect was inhibited by SAHA. The oxaliplatin‑induced Src phosphorylation was not impaired with Akt inhibition. In conclusion, oxaliplatin and SAHA exhibited a positive interaction when used in combination and were found to suppress gastric cancer cell survival and growth. The reversal of oxaliplatin‑induced Src activation may be responsible for this positive interaction.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Osteosarcoma, which is the most common type of highly malignant bone tumor in children and adolescents, has poor diagnosis and 2-year survival rates of 15-20% following surgery or radiotherapy, and has therefore generated marked attention. In order to investigate the potential biomarkers for diagnosing osteosarcoma, the expression profiling data from normal and disease tissues were compared, respectively, and the differentially‑expressed genes were analyzed by three different statistical tests. Interacting proteins were determined and an interaction network was constructed by Search Tool for the Retrieval of Interacting Genes database. Subsequently, the protein interaction network was decomposed and Gene Otology annotation using Cytoscape, Mcode and Bingo, was conducted on the function modules. Finally, three differentially‑expressed genes GJA1, COL1A2 and COL5A2 were identified, and an interaction network was successfully generated with COL1A2 and COL5A2 at the core. From the results, it was observed that COL1A2 and COL5A2 interact with a number of genes of the matrix metalloprotease (MMP) family, including MMP1, MMP2, MMP3 and MMP14, TGFβ and RUNX2. Furthermore, these genes have been confirmed to be important in the tumorigenesis of osteosarcoma. It was hypothesized that the upregulation of the COL gene family may be considered as a diagnostic marker for osteosarcoma and collagen may be administered as a therapy.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: Heat shock factor 1 (HSF1) is associated with tissue‑specific tumorigenesis in a number of mouse models, and has been used a as prognostic marker of cancer types, including breast and prostatic cancer. However, its role in human hepatocellular carcinoma (HCC) is not well understood. Using immunoblotting and immunohistochemical staining, it was identified that HSF1 and its serine (S) 326 phosphorylation, a biomarker of HSF1 activation, are significantly upregulated in human HCC tissues and HCC cell lines compared with their normal counterparts. Cohort analyses indicated that upregulation of the expression of HSF1 and its phospho‑S326 is significantly correlated with HCC progression, invasion and patient survival prognosis (P<0.001); however, not in the presence of a hepatitis B virus infection and the expression of alpha-fetoprotein and carcinoembryonic antigen. Knockdown of HSF1 with shRNA induced the protein expression of tumor suppressor retinoblastoma protein, resulting in attenuated plc/prf5 cell growth and colony formation in vitro. Taken together, these data markedly support that HSF1 is a potential prognostic marker and therapeutic target for the treatment of HCC.
    Molecular Medicine Reports 09/2014;
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    ABSTRACT: To investigate the effects of subminimum inhibitory concentrations of cephalosporins on bacterial biofilm formation, the biofilm production of 52 Escherichia (E.) coli strains was examined following treatment with cephalosporin compounds at 1/4 minimum inhibitory concentrations (MICs). Ceftazidime (CAZ) inhibited biofilm formation in seven isolates, while cefoperazone (CFP) enhanced biofilm formation in 18 isolates. Biofilm formation of E. coli E42 was inhibited by CAZ and induced by CFP. Therefore, using reverse transcription‑polymerase chain reaction, the expression of the biofilm‑modulating genes of this isolate was investigated. To monitor the production of the autoinducer of quorum sensing in E. coli, autoinducer‑2 (AI‑2) production was detected by measuring the bioluminescence response of Vibrio harveyi BB170. Antisense oligonucleotides (AS‑ODNs) targeting S‑ribosylhomocysteine lyase (luxS) inhibited the expression of the luxS gene in E. coli. CAZ at 1/4 MIC reduced luxS mRNA levels and the production of AI‑2, whereas CFP at 1/4 MIC had the opposite effect. AS‑ODNs targeting luxS significantly decreased the aforementioned inhibitory effects of CAZ and the induction effects of CFP on E. coli biofilm formation. Therefore, biofilm formation by the E. coli clinical isolate E42 was evoked by CFP but attenuated by CAZ at sub‑MICs, via a luxS/AI‑2‑based quorum sensing system.
    Molecular Medicine Reports 09/2014;

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