Molecular Medicine Reports (Mol Med Rep )

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Impact factor 1.48

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    Impact factor
  • 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

  • Molecular Medicine Reports 01/2015; in press.
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    ABSTRACT: The zebrafish (Danio rerio) is a useful vertebrate model for use in cardiovascular drug discovery. The present study aimed to construct optimized methods for the study of intravascular lipid metabolism of zebrafish. The lipophilic dye, Oil Red O, was used to stain fasting zebrafish one to eight days post-fertilization (dpf) and to stain 7-dpf zebrafish incubated in a breeding system containing 0.1% egg yolk as a high-fat diet (HFD) for 48 h. Three-dpf zebrafish were kept in CholEsteryl boron-dipyrromethene (BODIPY) 542/563 C11 water for 24 h which indicated the efficiency of CholEsteryl BODIPY 542/563 C11 intravascular cholesterol staining. Subsequently, 7-dpf zebrafish were incubated in water containing the fluorescent probe CholEsteryl BODIPY 542/563 C11 and fed a high-cholesterol diet (HCD) for 10 d. Two groups of 7-dpf zebrafish were incubated in regular breeding water and fed with a regular or HCD containing CholEsteryl BODIPY 542/563 C11 for 10 d. Finally, blood lipids of adult zebrafish fed with regular or HFD for seven weeks were measured. Oil Red O was not detected in the blood vessels of 7-8-dpf zebrafish. Increased intravascular lipid levels were detected in 7-dpf zebrafish incubated in 0.1% egg yolk, indicated by Oil Red O staining. Intravascular cholesterol was efficiently stained in 3-dpf zebrafish incubated in breeding water containing CholEsteryl BODIPY 542/563 C11; however, this method was inappropriate for the calculation of intravascular fluorescence intensity in zebrafish >7‑dpf. In spite of this, intra-aortic fluorescence intensity of zebrafish fed a HCD containing CholEsteryl BODIPY 542/563 C11 was significantly higher (P<0.05) than that of those fed a regular diet containing CholEsteryl BODIPY 542/563 C11. The serum total cholesterol and triglyceride levels of adult zebrafish fed a HFD were markedly increased compared to those of the control group (P<0.05). In conclusion, the use of Oil Red O staining and CholEsteryl BODIPY 542/563 C11 may have applications in zebrafish intravascular lipid metabolism research and screens for novel lipid-regulating drugs.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: The aim of this study was to investigate the role of the complement regulatory protein cluster of differentiation 55 (CD55) in the pathogenesis of diabetic neuropathic pain (DNP). Healthy adult male C57BL/6J mice were intraperitoneally injected with streptozotocin (STZ) in order to induce DNP. Peripheral blood glucose and protein, and the mRNA expression levels of C3 and CD55 in the spinal cord were determined. In addition, the behaviors of these mice were observed. The results showed that STZ‑treated mice displayed the clinical manifestations of diabetes mellitus, and that their peripheral blood glucose was markedly increased. On the 21st and 28th days following the STZ injection, the mechanical pain threshold and thermal pain threshold of the mice were dramatically reduced (P<0.05). |Additionally, 14 days post‑STZ injection, the mRNA expression of C3 in the spinal cord was significantly increased, which continued for 28 days. On the 21st and 28th days, the number of C3 positive cells in the spinal cord was markedly increased. Seven days after the STZ injection, the number of cells positive for CD55 was markedly reduced in the spinal dorsal horn and subsequently remained at a low level. The mRNA expression of CD55 also was significantly reduced (P<0.05) and remained so for 28 days. The reduction in the expression levels of CD55 occurred earlier than the changes in the expression of C3, suggesting that the downregulation of CD55 expression precedes, and has an important role regarding, the activation of C3 in the occurrence and development of DNP.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: Klotho is a novel anti-aging hormone involved in human coronary artery disease. The present study aimed to detect the effects and mechanism of Klotho on cardiomyocytes in a hypoxia/reoxygenation (H/R) model in vitro. Neonatal Sprague-Dawley rat cardiomyocytes were randomly distributed into experimental groups as follows: Control group; H/R group, 4‑h hypoxia followed by 3‑h reoxygenation; and H/R+Klotho group, incubated with 0.1, 0.2 or 0.4 µg/ml Klotho protein for 16 h and then subjected to 4‑h hypoxia/3‑h reoxygenation. In order to evaluate cardiomyocyte damage, cell viability and lactate dehydrogenase (LDH) levels were measured. Cell apoptosis was measured by flow cytometry. The 2',7'-dichlorofluorescein diacetate reagent was used to estimate the intracellular generation of reactive oxygen species (ROS). Immunofluorescence staining was used to test whether Klotho induced decreased nuclear translocation of forkhead box protein O1 (FOXO1). Western blot analysis was performed to detect protein levels of FOXO1, phospho-FOXO1, Akt, phospho-Akt and superoxide dismutase 2 (SOD2). Cell viability was significantly decreased, levels of LDH in the cardiomyocyte culture medium were significantly increased and the apoptotic rate was enhanced in the H/R group when compared with those of the control group. Compared with the H/R group, cell viability of the H/R+Klotho groups was significantly higher (P<0.05). Treatment with Klotho protein resulted in a significant resistance of cardiomyocytes to apoptosis and the release of LDH was decreased. Intracellular ROS levels in the H/R group were significantly elevated above those of the control group (P<0.05). Following treatment with Klotho, intracellular ROS levels were significantly decreased compared with those of the H/R group (P<0.05). Western blot analysis confirmed that Klotho protein treatment increased FOXO1 levels in the nucleus and decreased FOXO1 levels in the cytoplasm. Furthermore, exogenous Klotho protein promoted translocation of FOXO1 from cytoplasm to nucleus. In addition, the administration of Klotho protein suppressed phosphorylation of FOXO1 and Akt, and markedly increased the protein expression levels of SOD2. In conclusion, treatment with Klotho protein had beneficial effects on cardiomyocytes undergoing H/R injury. The mechanism of this effect may be associated with suppressed apoptosis of cardiomyocytes, inhibition of phosphorylation of FOXO1 and Akt as well as suppression of cytoplasm transfer of FOXO1.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: Accumulating evidence suggests that β‑catenin signaling may be involved in oral tongue squamous cell carcinoma (OTSCC) cell invasion. Abnormal activation of twist‑related protein 1 (TWIST1 or TWIST) has been identified in several types of human cancer. A recent study showed that overexpression of TWIST is associated with a poor prognosis in patients with OTSCC and may enhance OTSCC cell invasion. This study investigated the effect of TWIST on β‑catenin signaling in OTSCC cells and its impact on OSTCC cell invasion. Stable overexpression of TWIST, with or without knockdown of β‑catenin, and stable knockdown of TWIST were performed in SCC‑4 and TCA8113 human OTSCC cells. Overexpression of TWIST in SCC‑4 and TCA8113 cells increased β‑catenin signaling luciferase reporter activity, mRNA levels of the β‑catenin signaling target genes, c‑Myc and c‑Jun levels, soluble β‑catenin level, the phosphorylation status of glycogen synthase kinase‑3β (GSK‑3β) at serine 9, matrix metalloproteinase‑2 (MMP‑2) expression and cell invasion. Knockdown of TWIST had the opposite effect. All of these changes, with the exception of phosphorylation of GSK‑3β, were eliminated by stable knockdown of β‑catenin. In addition, the phosphatidylinositol 3‑kinase (PI3K) inhibitor, LY294002 abrogated the enhancing effects of TWIST on mRNA levels of c‑Myc and c‑Jun, soluble β‑catenin levels, MMP‑2 expression, cell invasion and GSK‑3β phosphorylation. In conclusion, the present study demonstrated that TWIST enhances cell invasion and MMP‑2 expression in OTSCC cells through β‑catenin signaling, probably via a PI3K‑dependent mechanism. This study provides novel insights into the molecular mechanisms underlying OTSCC progression.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: The aim of the present study was to explore the effect of hypoxia on ovarian cancer. A total of 6 samples were analyzed: SKOV3‑IP cells (ovarian cancer cell line); SKOV3‑IP and regulatory T (Treg) cells; SKOV3‑IP and cytotoxic T lymphocytes (CTLs); SKOV3‑IP and natural killer (NK) cells; SKOV3‑IP co-cultured with CTLs and Treg cells; and SKOV3‑IP co-cultured with Treg cells and NK cells. The expression of indoleamine 2,3‑dioxygenase (IDO) was detected by reverse transcription-polymerase chain reaction (RT‑PCR) and western blot analysis. An enzyme‑linked immunosorbent assay (ELISA) was used to detect the concentration of transforming growth factor‑β (TGF‑β), interferon‑γ (IFN‑γ), interleukin‑2 (IL‑2), interleukin‑10 (IL‑10), and perforin. Moreover, ovarian cancer cell apoptosis and invasive ability were examined using flow cytometry and a Transwell chamber assay. IDO expression was significantly reduced in hypoxia and enhanced by Treg cells. Treg cells inhibited the IL‑2, IFN‑γ and perforin secretion, and significantly (P<0.05) increased the IL‑10 and TGF‑β levels. The effects of Treg cells were enhanced with prolongation of the cell exposure to hypoxic conditions. In addition, Treg cells attenuated the promotive effect of CTLs and NK cells on cancer cell apoptosis. In addition, Treg cells significantly increased the SKOV3‑IP invasive ability (P=0.00109) under hypoxic conditions. Our results suggest that IDO and Treg cells may serve as important therapeutic targets for patients with ovarian cancer.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: MacroH2A is a histone modification factor the activity of which has been acutely studied in cancer progression, and a number of studies have shown that the progression of certain types of cancer is under regulation by MacroH2A. However, information regarding the underlying molecular mechanisms of MacroH2A inhibition on the cell cycle remains elusive, and elucidating this process may aid in the production of novel treatment strategies. The aim of the current study was to investigate the inhibitory effects of MacroH2A on osteosarcoma cell progression, and the possible molecular mechanisms of this process. MacroH2A overexpression and interference vectors were designed and transfected into U2‑OS osteosarcoma cells. The cells underwent reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), western blot analysis and immunofluorescence assays. The apoptosis rate and cell cycle stage were assayed using flow cytometry. The results revealed that the overexpression of MacroH2A inhibited the progression of U2‑OS osteosarcoma cells, and the cells were arrested at the G2/M stage of the cell cycle. The molecular mechanism by which MacroH2A suppresses the cell progression involves the inhibition of the expression of cyclin D and cyclin‑dependent kinase (CDK) genes, including cyclin D1, cyclin D2, CDK4, CDK6 and CDK8. Taken together, the present results revealed that MacroH2A is an important modifier of chromatin that downregulates the progression of osteosarcoma cells and triggers disturbance of the cell cycle via the downregulation of cyclin D and CDK genes.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: The aim of this study was to determine if heightened stress had an adverse affect on the postural control of 14 young right‑handed females during quiet standing in either the presence or the absence of visual input. The level of stress was evaluated by measuring the free cortisol response to awakening (cortisol awakening response; CAR) and by employing the perceived stress scale (PSS). Overall mood disturbance was measured using the profile of mood states (POMS). Postural control was evaluated using a force platform by measuring the 95% confidence ellipse area described by the center of pressure during 5 balance positions maintained for at least 52 sec, each with open and closed eyes. The results of this study revealed a significant positive correlation between CAR, PSS and POMS for each of the studied subjects. Furthermore, it was observed that whilst the level of stress was capable of influencing postural stability, this influence was particularly evident when no visual information was available. Additionally, it was determined that maintenance of posture is easier when the dominant foot is ahead, regardless of visual input.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: The cell cycle is tightly regulated by the family of cyclin-dependent kinases (CDKs). CDKs act as regulatory factors on serine and threonine residues by phosphorylating their substrates and cyclins. CDK‑targeting drugs have previously demonstrated promising effects as cancer therapeutics both in vitro and in vivo. Roscovitine, a purine‑derivative and specific CDK inhibitor, has been demonstrated to arrest the cell cycle and induce apoptosis in a number of different cancer cell lines, including HeLa cervical cancer cells. In the present study, roscovitine was able to decrease both the cell viability and cell survival as well as induce apoptosis in a dose‑dependent manner in HeLa cells by modulating the mitochondrial membrane potential. The decrease of anti‑apoptotic B-cell lymphoma 2 (Bcl‑2) and Bcl-2 extra large protein expression was accompanied by the increase in pro‑apoptotic Bcl-2-associated X protein and P53-upregulated modulator of apoptosis expression. The marked decrease in Bcl‑2 following exposure to roscovitine (20 µM) for 48 h prompted us to determine the autophagic regulation. The outcome revealed that roscovitine triggered Beclin‑1 downregulation and microtubule-associated light chain 3 cleavage starting from 12 h of incubation. Another biomarker of autophagy, p62, a crucial protein for autophagic vacuole formation, was diminished following 48 h. In addition, monodansyl cadaverin staining of autophagosomes also confirmed the autophagic regulation by roscovitine treatment. The expression levels of different Bcl‑2 family members determined whether apoptosis or autophagy were induced following incubation with roscovitine for different time periods. Downregulation of pro‑apoptotic Bcl‑2 family members indicated induction of apoptosis, while the downregulation of anti‑apoptotic Bcl‑2 family members rapidly induced autophagosome formation in HeLa cells.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: GYY4137 is a water‑soluble, small molecule hydrogen sulfide (H2S)‑release agent that possesses potent cardioprotective and anti‑inflammatory properties in experimental models. Coxsackie virus B3 (CVB3) infection commonly causes viral myocarditis, which mainly involves immune cell infiltration, eventually resulting in heart failure. In the present study, the effects and underlying mechanisms of GYY4137 treatment of CVB3‑induced myocarditis were investigated. The effects of GYY4137 on CVB3‑induced nuclear factor‑kappa B (NF‑κB) activity were examined by western blotting, immunofluorescence and electrophoretic mobility shift assay. Mitogen‑activated protein kinase (MAPK) signaling protein expression levels were detected by western blotting. Cardiomyocyte damage‑related enzyme activities, such as lactate dehydrogenase (LDH) and creatine kinase MB (CK‑MB), were measured by ELISA, as well as the production of proinflammatory cytokines. The results revealed that GYY4137 suppressed CVB3‑induced secretion of LDH, CK‑MB and pro‑inflammatory cytokines, such as tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6. Furthermore, the activation of NF‑κB and the IκBα degradation induced by CVB3 were also inhibited by GYY4137. Notably, the phosphorylation of p38, ERK1/2 and JNK1/2 induced by CVB3 was also inhibited by GYY4137. In conclusion, the data demonstrate that GYY4137 exerts anti‑inflammatory effects in CVB3‑infected cardiomyocytes. This anti‑inflammatory mechanism may be associated with suppression of NF‑κB and MAPK signaling pathway activation.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: The objective of the present study was to search for Msh homeobox 1 (MSX1), paired box gene 9 (PAX9), ectodysplasin‑A (EDA) and axis inhibition protein 2 (AXIN2) variants in a family with isolated oligodontia and analyse the pathogenesis of mutations that result in oligodontia phenotypes. Members of a single family (but of different descent) with oligodontia and unrelated healthy controls were enrolled in our study. Genomic DNA was isolated from blood samples. Mutation analysis was performed by amplifying MSX1, PAX9, EDA and AXIN2 exons as well as their exon‑intron boundaries and sequencing the products. DNA sequencing of the AXIN2 gene revealed three mutations in the two patients with oligodontia: a homozygotic silent mutation c.1365A>G (p.Pro455=) in exon 3, two c.956+16A>G mutations (II‑1: homozygosis; III‑1: heterozygosis) and c.1200+71A>G (homozygosis) in the intron, which possibly contributed to structural and functional changes in proteins. The heterozygotic mutations c.1365A>G and c.1200+71A>G were identified in the proband's mother (II‑2). No mutations were detected in the MSX1, PAX9 and EDA genes of oligodontia patients. The findings suggest that the c.956+16A>G, c.1365A>G and c.1200+71A>G mutations of AXIN2 may be responsible for the oligodontia phenotype in this family, but these findings require further study.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: microRNAs (miRNAs) are small, non‑coding RNAs that inhibit the expression of target protein coding genes at the post‑transcriptional level. miR‑122 is a liver specific miRNA. Notably, miR‑122 is used by the hepatitis C virus (HCV) for triggering viral replication by interacting with the 5' untranslated region of the HCV RNA. The present study demonstrated that miR‑122 inhibited the expression of signal transducer and activator of transcription 3 (STAT3), an antivirus response repressor. The HCV RNA acted as an 'miRNA sponge', which upregulated the expression of STAT3 by sealing miR‑122. Subsequently, it was confirmed that this miR‑122 sponge function of HCV RNA repressed the expression of polyinosinic‑polycytidylic acid‑stimulated type I interferons. The present study provided a deeper understanding of the complex role of miR‑122 in the progression of HCV infection and supported the miR‑122 inhibition strategy in anti‑HCV infection treatment.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: MicroRNAs (miRNAs) are single‑stranded RNA species that constitute a class of non‑coding RNAs, and are emerging as key regulators of gene expression. Since each miRNA is capable of regulating multiple genes, miRNAs are attractive markers for studies of coordinated gene expression. In this study, we investigated miRNA expression profiling using a massively parallel sequencing technique to compare non‑small‑cell lung cancer (NSCLC) tissue and normal lung tissue. Lung cancer tissue and normal lung tissue were obtained from nine NSCLC patients. RNA isolated from these samples was processed using RNA sequencing (RNA Seq) and the HiSeq 2000 system. Differentially expressed miRNAs and mRNAs were analyzed using a t‑test. We selected target pairs that showed a negative correlation among significantly differentially expressed miRNAs and their putative target mRNAs using miRBase Targets. The differences in the expression levels of 222 miRNAs and 1,597 genes were statistically significant, as indicated by an absolute fold change ≥1.5 and P<0.05. miR‑577, miR‑301b, miR‑944, miR‑891a and miR‑615‑3p were generally upregulated, and miR‑338‑3p was generally downregulated. miRNA‑mRNA target pair analysis revealed that 49 miRNAs had 696 target mRNAs. There were significantly differentially expressed miRNAs and mRNAs between lung cancer and normal tissue. Further investigation of miRNAs and their target genes is warranted to better understand NSCLC.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: Dihydromyricetin (DHM) is a flavonoid compound which possesses potent antitumor activity. In the present study, it was demonstrated that DHM significantly inhibited proliferation and induced apoptosis in mouse hepatocellular carcinoma Hepal‑6 cells. Transforming growth factor β (TGF‑β) is recognized as a major profibrogenic cytokine and is therefore a common target for drugs in the treatment of liver disease. The present study aimed to investigate whether TGF‑β was involved in DHM‑triggered cell‑viability inhibition and apoptosis induction. An MTT assay was used to evaluate the viability of Hepal‑6 cells following DHM treatment. TGF‑β signalling is mediated by Smads and nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) is a crucial regulator of reactive oxygen species ROS production. TGF‑β, Smad3, phosphorylated (p)‑Smad2/3 and NOX4 protein expression levels were evaluated by western blot analysis. TGF‑β and NOX4 gene expression levels were determined by quantitative polymerase chain reaction. The results indicated that DHM downregulated TGF‑β, Smad3, p‑Smad2/3 and NOX4 in a concentration‑dependent manner. A cell counting assay indicated that DHM also inhibited Hepal‑6 cell growth in a concentration‑dependent manner. TGF‑β expression was significantly decreased following DHM treatment. In conclusion, the results of the present study defined and supported a novel function for DHM, indicating that it induced cell apoptosis by downregulating ROS production via the TGF‑β/Smad3 signaling pathway in mouse hepatocellular carcinoma Hepal‑6 cells.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: A number of studies have shown that baicalein shows high antitumor activity in vitro and in vivo. In this study, the inhibitory effect of baicalein on human cervical cancer HeLa cells was studied in vitro. HeLa cells were treated with high (100 µg/ml) and low (50 µg/ml) doses of baicalein, and cell growth inhibition rates were examined by the MTT assay. The morphological changes of apoptotic cells were observed under the light and electron microscope, while the rate of cell apoptosis was examined by flow cytometry. The expression of apoptosis-related proteins was analyzed by western blot, and caspase-3 activation was examined by a caspase-3 activity assay and spectrophotometry. The results demonstrated that baicalein inhibits the proliferation of HeLa cells and induces apoptosis in a caspase-3-dependent pathway, through downregulation of the B-cell lymphoma 2 (Bcl-2) protein and upregulation of the Bcl-2-associated X protein (Bax), Fas, Fas ligand (FasL) and caspase-8. Thus, we conclude that baicalein induces apoptosis of HeLa cells via the mitochondrial and the death receptor pathways. Cell apoptosis in HeLa cells was most likely promoted by the activation of the proteolytic enzyme caspase-3 in both pathways.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: Numerous lines of evidence previously indicated that conserved dopamine neurotrophic factor (CDNF) has potential therapeutic value for Parkinson's disease (PD); however, this hypothesis remains controversial. In the present study, the therapeutic effects of engineered CDNF-expressing bone marrow stromal cells (CDNF-BMSCs) on dopaminergic (DA) neurons were evaluated in vivo. CDNF-BMSCs and control BMSCs were transplanted into the rat striatum and one week later, 6-hydroxydopamine (6-OHDA) was administered to induce neurotoxicity. It was discovered that intrastriatal transplantation of CDNF-BMSCs significantly reduced 6-OHDA-induced neurotoxicity in DA neurons with regard to behavioral recovery and tyrosine hydroxylase levels in the substantia nigra and striatum. These data therefore indicated that transplantation of engineered CDNF-BMSCs into the striatum may present a beneficial strategy for the treatment of PD.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: microRNAs (miRNAs) have been demonstrated to be important gene regulators with critical roles in diverse biological processes, including tumorigenesis. Accumulating evidence suggests that miR‑338-3p exerts a tumor suppressor role and is downregulated in tumors, including gastric cancer and colorectal carcinoma. However, the role of miR‑338-3p in lung cancer, particularly non‑small‑cell lung carcinoma (NSCLC), has remained elusive. In the present study, the expression levels of miR‑338-3p in NSCLC tissues were compared with those of matched normal tissues by use of polymerase chain reaction analysis. miR-338-3p was shown to be downregulated in NSCLC tissues, and the expression levels of miR‑338‑3p were significantly correlated with NSCLC cancer differentiation, pathological stage and lymph‑node metastasis. Ectopic miR-338-3p expression significantly suppressed the in vitro proliferation and colony formation of NSCLC cells and enhanced apoptosis. Of note, ectopic miR‑338-3p expression significantly inhibited Ras‑related protein 14 (RAB14) mRNA and protein expression, and reduced luciferase reporter activity containing the RAB14 3'-untranslated region through the first binding site. These findings suggested that miR‑338-3p regulated the survival of NSCLC cells partially through the downregulation of RAB14. Therefore, targeting the miR‑338-3p/RAB14 interaction may serve as a novel therapeutic application to treat NSCLC patients.
    Molecular Medicine Reports 11/2014;
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    ABSTRACT: Lingqi capsules (LQCs) are commonly used in Chinese herbal medicine to support the immune system and inhibit tumor growth. The capsules are considered to have a direct effect on tumor cell proliferation and support tumor cell apoptosis. In the present study, the effects of LQC serum on the colorectal cancer cell line, LoVo, and on tumors induced by the cell line were investigated in nude mice. LQC serum was generated by feeding Wistar rats LQC and isolating the serum from blood samples obtained from the rats. The serum was then used to treat LoVo cells for 24, 48 and 72 h, after which the cell morphology and proliferation were assessed. In addition, nude mice were injected with 0.2 ml LoVo cells subcutaneously to produce tumors. After 24 h, xenografted nude mice were treated with 5.0, 2.5 or 1.25 g/kg/day LQC serum by gavage for 21 days and the tumor growth, morphology, apoptosis of tumor cells and expression profiles of hepatocyte growth factor (HGF) and its receptor, c‑Met, were investigated. Compared with the negative controls, inhibition of cell growth was clearly visible in the LoVo cells treated for 24, 48 and 72 h and this inhibition was enhanced as the exposure time and drug concentration increased. The growth of solid tumors induced by the transplantation of LoVo cells into nude mice was inhibited to differing degrees. Following LQC treatment, the apoptotic rates of the cells were increased, the protein and mRNA expression levels of HGF were downregulated and those of c‑Met were upregulated. These findings suggest that LQC treatment inhibits colorectal cancer by downregulating the HGF/c‑Met signal transduction pathway.
    Molecular Medicine Reports 11/2014;