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Introduction: Cancer is a complex disease in which gene expression changes. This study was conducted with the aim of investigating the effects of MT1JP lncRNA in controlling lung cancer cells. Material & Methods: TC-1 [JHU-1] cells were transfected with pcDNA3.1(+)- MT1JP, Plko.1-EGFP-PURO-siRNA and empty plasmids, and the expression of MT1JP gene and siRNA fragment was confirmed by RT-PCR reaction. The role of MT1JP in migration was investigated by scratch assay and apoptosis by flow cytometry. The expression change of candidate genes involved in apoptosis and cell proliferation (Bim, AKT, Bax and Bcl-2) was evaluated by q-PCR reaction. Findings: The results showed that the expression of Bim gene showed a significant increase in the presence of high expression of MT1JP, while the expression of Bim gene decreased significantly with silencing of MT1JP by siRNA. The expression of Bax and Bcl-2 genes showed a significant increase and decrease, respectively, in the presence of high expression of MT1JP. In the cells transfected with pcDNA3.1(+)- MT1JP, the AKT gene showed a decrease in expression, and on the other hand, in the cells transfected with siRNA, the AKT gene had a significant increase in expression (p < 0.05). Also, the scratch assay results showed that MT1JP lncRNA has an inhibitory role on cell migration. Flow cytometry data showed that transfection by pCDNA3.1(+)-MT1JP could increase cell apoptosis levels. Discussion & Conclusion: The present study showed that lncRNA MT1JP inhibits cell proliferation and migration and at the same time increases apoptosis of TC-1 [JHU-1] cells. This study may help improve our understanding of lung cancer; however further studies are needed. [ABSTRACT FROM AUTHOR]

Introduction: The increasing trend of cancer morbidity and mortality is a major human health concern, indicating the necessity for the design and introduction of novel anticancer compounds. The use of nanotechnology products is a new approach to cancer treatment. Therefore, the current study was performed to synthesize Titanium Dioxide nanoparticles (NPs) functionalized with glutamine and conjugated to Thiosemicarbazide (TiO2@Gln-TSC) to inhibit the proliferation of liver cancer cells line (HepG2) and evaluate the effect of TiO2@Gln-TSC NPs on the expression of apoptotic genes. Material & Methods: TiO2@Gln-TSC NPs were synthesized by a chemical method and characterized by Fourier-transform infrared spectroscopy (FT-IR), Energy-dispersive X-ray spectroscopy (EDS), Scanning electron microscopy (SEM), and Transmission electron microscopy (TEM). The cytotoxicity of the Titanium Dioxide nanoparticles was evaluated by the MTT assay, and relative gene expression was studied by Real Time PCR method. Findings: The results showed that the synthesized Titanium Dioxide nanoparticles were spherical with a size range of 59 to 82 nm. The particles had a considerable anti-proliferative effect on liver cancer cells line with IC50 of 80 µg/mL. The treatment of the cancer cell line with TiO2@Gln-TSC NPs significantly increased the expression of the CASP3, BAX, and BCL2 by 2.8, 2.7, and 1.3 folds, respectively, which indicated the activation of apoptotic pathways in the treated cells. Discussion & Conclusion: The results showed that the TiO2@Gln-TSC NPs could inhibit the proliferation of liver cancer cells line and by triggering the apoptosis pathway. [ABSTRACT FROM AUTHOR]

Background and Aim This study aimed to investigate the association between Endoplasmic Reticulum autophagy (ER-phagy) and Alzheimer’s Disease (AD) by analyzing the expression patterns of related genes in animal models. Methods & Materials Microarray data of AD patients’ brain tissues were extracted from the Gene Expression Omnibus (GEO) database. These data were first analyzed in GEO2R online tool. Then, the expression of ER-phagy related genes were isolated and the protein interaction networks were plotted by STRING database for the genes with increased expression. Finally, the relationship between the genes that had significant increased expression were designed, and the expression of new identified genes in each study was examined. Ethical Considerations All ethical principles were considered in this article. Results Genes involved in ER-phagy showed a sporadic expression in different AD models. An increase in the expression of ER-phagy regulatory 1 (FAM134B) gene was observed in studies with the mutation in both Microtubule-associated Protein Tau (MAPT) and Amyloid Precursor Protein (APP) genes. Increase in the expression of NPC intracellular cholesterol transporter 1 (NPC1) gene was observed in two studies that had mutations in APP, Presenilin 1 (PSEN1) and MAPT genes. Moreover, SEC62 homolog and Cell Cycle Progression 1 (CCPG1) genes both showed decreased expression in one study. Finally, the expression of Reticulon 3 (RTN3) was not significant in any of the studies. Conclusion The genes involved in ER-phagy have a sporadic expression in AD models, where only two genes FAM134B and NPC1 are involved in AD. The FAM134B gene seems to interact with the Wnk1 gene, which plays a role in cell survival and proliferation, in the hippocampus and forebrain. It also interacts with the Map1lc3b gene, which has a role in phagosome deletion and protein ubiquitination, in the forebrain. It also interacts with the Map1lc3b gene, which has a role in phagosome deletion and protein ubiquitination, in the forebrain. NPC1 had interaction with the Abcg1 gene, which activates lipid homeostasis, in the subventricular zone. [ABSTRACT FROM AUTHOR]

Background and Objective: Some problems such as low viability and apoptosis after injection to the body because of exposure to toxic factors such as hypoxia, thermal stress, oxidative stress and food deprivation are encountered with stem cell application. It is suggested that preconditioning of the cells with cytotoxic factors before injection could enhance their efficiency. This study was done to determine the mesenchymal stem cell proliferation exposed to hypoxia by cobalt chloride. Methods: In this experimental study, Mesenchymal stem cells were isolated from rat bone marrow and cultured at least for four times. The cells were cultured in 96 well plates and treated with different concentration (0, 5, 10, 20, 50, 70, 90, 100, 120, 150 and 200 μM) of cobalt chloride for 6, 12, 24 and 46 hours. Cell proliferation was detected by MTT assay [3-(4,5-Dimethylthiazol-2-Yl)-2,5- Diphenyltetrazolium Bromide]. Results: The cells isolated from bone marrow were propagated easily in culture condition. The cells morphology was not altered after exposure to cobalt chloride. Preconditioning of mesenchymal stem cells with 120 μM for 6 hours, 20μM for 12 and 24 hours and 5μM for 48 hours significantly improved cell proliferation after hypoxia in cell culture (P<0.05). Conclusion: Hypoxia preconditioning increases proliferation of mesenchymal stem cell. [ABSTRACT FROM AUTHOR]

Background and Objective: Sphingosine-1-phosphate (S1P) is involved in regulation of proliferation, differentiation, hypertrophy and anti-apoptosis and activation of satellite cells. This study was done to evaluated the effect of 8 weeks resistance training on sphingosine-1-phosphate level and gene expression of SK1 enzyme, isoforms of MHCs in skeletal muscles of male Wistar rats. Materials and Methods: This experimental study was done on Twenty four 8-week-old 190-250 gr male Wistar rats. The rats were allocated randomly into control (N=12) and training (N=12) groups. Resistance training was done using a 1 meter height ladder with 2 cm grid with an 85 degree incline, and weights attached to rat's tails. The content of S1P present in the chloroform layer was determined by means of high performance liquid chromatography (HPLC). Determination of relative mRNA expression was performed by Real-time PCR. Data were analyzed using SPSS-17, Kolmogorov-Smirnov and independent t-test. Results: Resistance exercise training increased the total content of S1P in FHL (fast-twitch) and soleus (slow-twitch) muscles in comparison with control group (P<0.05). Resistance exercise training changed the gene expression of FHL SK1, SOL SK1, FHL MHC I, Sol MHC I, FHL MHC IIa, Sol MHC IIa, FHL MHC IIb, Sol MHC IIb, FHL MHC IIx, Sol MHC IIx in comparison with control group (P<0.05). Conclusion: This study showed that S1P level and gene expression of SK1, MHCs increased at skeletal muscles after training. [ABSTRACT FROM AUTHOR]

Background and Objective: Research have been focused on the applying the chemical inducer for trans-differentiation the adult BMSCs into neural cell. So that, at the first should investigate the toxcity effect of the chemical inducer on the induced cells. Plasticity and easy accessibility of bone marrow mesenchymal stem cells is a unique charactristic for treatment of neural disorderies. This study was desgined to determine the inductive effect of Deprenyl and Dimethyl sulfoxide on proliferation and survival of the mesenchymal stem cells. Materials and Methods: In this experimental study, BMSCs isolated from the adult rat bone marrow and cultured in αMEM containing 10% FBS. Cell identity for surface antigens was performed in third passage by immunocytochemistry and multipotancy capacity of BMSCs was done by BMSC differentiation into adipocytes and osteocytes. The cells were exposed to chemical agents (a: the αMEM medium supplemented with 2% DMSO, b: the αMEM medium supplemented with 10-8M Deprenyl) for 24 houres and then transferred to αMEM containing 10% FBS cell survival and proliferation was evaluated after the 24, 48, 72 and 96 houres by MTT [3-(4-5-Dimethylthiazolyl-2-y1)-2,5-diphenyltetrazolium bromid] test. Data were analyzed using SPSS-16, One-Way ANOVA and Tukey tests. Results: In addition to expression the surface antigens and adipogenic and osteogenic differentiation by BMSCs, MTT test results showed that proliferation and survival of induced-deprenyl and DMSO cells within 48, 72 and 96 hours after the induction was increased significantly than negative control group. Conclusion: Deprenyl increases survival and cell proliferation compared to Dimethyl Sulfoxide. It can be used as cell inducer. [ABSTRACT FROM AUTHOR]

Background and Objective: Neurotrophic factors are diffusible polypeptides that have critical roles in survival, proliferation and differentiation of stem cells. This study was done to assess the role of neurotrophic factors (CNTF , BDNF, GDN F, NT- 3 ) expression and proliferation rate of neural stem cells (NSCs) in coculture with mesenchymal stem cells (MSCs). Materials and Methods: In this experimental study, NSCs and MSCs were isolated from adult Wistar rat. Initially, NSCs was harvested from temporal lobe after mechanical digestion by a sterile flamed Pasteur pipette and enzymatic digestion with trypsin and Dnase. The cell suspension was cultivated in a flask with DMEM/F12 medium supplemented with 10% FBS 100U/ml Penicillin and 100 mg/ml Streptomycin. To obtain MSCs, bone marrow of femur and tibia bones were flashed out and cultured. MSCs and NSCs cocultured by transwell system in DMEM/F12 medium supplemented with 10% FBS 100U/ml Penicillin and 100 mg/ml Streptomycin. Haemocytometer, immunocytochemistry and RT-PCR methods were performed to identify and evaluate cell proliferation, purity levels and neurotrophic factors expression. Results: There is no differences in NTFs profile of neurotrophic factors expression between coculture group and control NSCs, but interactions between MSCs and NSCs significantly promoted NSCs proliferation (P<0.05). Conclusion: This study showed that coculture of NSCs with MSCs might be prfered in cell-therapy than NSCs. [ABSTRACT FROM AUTHOR]