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1.
Int J Oncol ; 64(5)2024 May.
Article in English | MEDLINE | ID: mdl-38488025

ABSTRACT

Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 1D on p. 1134, the data panels showing the results for the 'Control' and '1 µmol/l GW9662' experiments (on the left hand side of the figure) were overlapping, such that these data had been derived from the same original source where they were intended to show the results from differently performed experiments. The authors were able to re­examine their original data, and realize that the data for the '1 µmol/l GW9662' panel had been selected incorrectly. The corrected version of Fig. 1, now featuring the correct data for the '1 µmol/l GW9662' experiment in Fig. 1D, is shown on the next page, The authors confirm their error did not grossly affect either the results of the conclusions reported in the paper, and are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum. They also apologize to the readership for any inconvenience caused. [International Journal of Oncology 46: 1131-1140, 2015; DOI: 10.3892/ijo.2015.2829].

2.
Mol Med Rep ; 13(1): 49-58, 2016 Jan.
Article in English | MEDLINE | ID: mdl-26572749

ABSTRACT

Recent studies regarding regenerative medicine have focused on bone marrow mesenchymal stem cells (BMSCs), which have the potential to undergo neural differentiation, and may be transfected with specific genes. BMSCs can differentiate into neuron­like cells in certain neurotropic circumstances in vitro. Basic fibroblast growth factor (bFGF) and nerve growth factor (NGF) are often used to induce neural differentiation in BMSCs in vitro. However, previous studies regarding their combined actions are insufficient. The present study is the first, to the best of our knowledge, to thoroughly assess the enhancement of neural differentiation of BMSCs following transfection with bFGF and NGF. Sprague­Dawley (SD) rat BMSCs were separated through whole bone marrow adherence, and were then passaged to the third generation. The cells were subsequently divided into five groups: The control group, which consisted of untransfected BMSCs; the plv­blank­transfected BMSCs group; the plv­bFGF­transfected BMSCs group; the plv­NGF­transfected BMSCs group; and the plv­NGF­bFGF co­transfected BMSCs group. Cell neural differentiation was characterized in terms of stem cell molecular expression, and the neuronal morphology and expression of neural­like molecules was detected in each of the groups. A total of 72 h post­transfection, the expression levels of neuron­specific enolase, glial fibrillary acidic protein, and nestin protein, were higher in the co­transfected group, as compared with the other groups, the expression levels of ß­tubulin III were also increased in the co­transfected cells, thus suggesting the maturation of differentiated neuron­like cells. Furthermore, higher neuronal proliferation was observed in the co­transfected group, as compared with the other groups at passages 2, 4, 6 and 8. Western blotting demonstrated that the transfected groups exhibited a simultaneous increase in phosphorylation of the AKT and extracellular signal­regulated kinases (ERK) signaling pathway. These results suggested that manipulation of the ERK and AKT signaling pathway may be associated with the differentiation of transfected BMSCs.


Subject(s)
Bone Marrow Cells/metabolism , Cell Differentiation , Fibroblast Growth Factor 2/genetics , Mesenchymal Stem Cells/cytology , Mesenchymal Stem Cells/metabolism , Nerve Growth Factor/genetics , Neurons/cytology , Animals , Blotting, Western , Cell Separation , Cell Shape , Extracellular Signal-Regulated MAP Kinases/metabolism , Female , Fibroblast Growth Factor 2/metabolism , Flow Cytometry , Genetic Vectors/metabolism , Glial Fibrillary Acidic Protein/metabolism , Humans , Immunophenotyping , Lentivirus/metabolism , Male , Nerve Growth Factor/metabolism , Phosphopyruvate Hydratase/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Rats, Sprague-Dawley , Transduction, Genetic , Transfection , Tubulin/metabolism
3.
Int J Oncol ; 46(3): 1131-40, 2015 Mar.
Article in English | MEDLINE | ID: mdl-25586304

ABSTRACT

The peroxisome proliferator-activated receptor γ (PPARγ) is emerging as an important regulator in various metabolic processes of cancer. Genistein, as a major isoflavonoid isolated from dietary soybean, possesses a wide variety of biological activities, particularly, in cancer prevention. However, the mechanisms by which genistein elicits its growth inhibiting effects in osteosarcoma (OS) MG-63 cells have not been extensively elucidated. MG-63 cells were treated for 2 days with various concentrations of genistein and/or GW9662 (a selective antagonist of PPARγ). The effect of different drugs on cell viability was determined by Cell Counting Kit-8 (CCK-8). The assay of cell proliferation was performed using 5-ethynyl-2'-deoxyuridine (EdU). The changes of apoptosis and cell cycle progression were detected by flow cytometry experiments. The protein expression of PPARγ pathway (PPARγ, PTEN, BCL-2, Survivin, P21WAF1/CIP1 and Cyclin B1) was determined by western blot analysis. The expression of PPARγ and PTEN mRNA was detected by real-time quantitative RT-PCR analysis. We report that genistein caused OS cell growth inhibition. We found that the PPARγ expression in OS cells increased after genistein treatment. Further studies on the mechanisms of genistein revealed a series of cell growth changes related to the PPARγ pathway; while cell cycle changes can be reversed by GW9662. Genistein plays an important role in preventing OS cell growth, which can impede the OS cell cycle as a non-toxic activator of PPARγ, providing novel insights into the mechanisms of the therapeutic activities of genistein.


Subject(s)
Anticarcinogenic Agents/pharmacology , Bone Neoplasms/pathology , Cell Proliferation/drug effects , Genistein/pharmacology , Osteosarcoma/pathology , PPAR gamma/metabolism , Anilides/pharmacology , Bone Neoplasms/genetics , Cell Line, Tumor , Cell Survival/drug effects , Cell Survival/genetics , Gene Expression Regulation, Neoplastic/drug effects , Humans , Osteosarcoma/genetics , PPAR gamma/antagonists & inhibitors , PPAR gamma/genetics , Signal Transduction/drug effects , Signal Transduction/genetics
4.
Biomed Res Int ; 2014: 931850, 2014.
Article in English | MEDLINE | ID: mdl-24757683

ABSTRACT

In this study effect of salvianolic acid B was observed on motor function recovery of rats with spinal cord injury. 50 rats were selected and after inducing SCI their recovery under controlled conditions was studied using Sal B and PBS (as control). Both compounds were introduced intraperitoneally in respective groups of traumatic rats at the same time intervals for 28 days. It was observed that Sal B introduced at 5 mg/kg/day resulted in better motor function recovery. BBB score was recorded which increased significantly along with the reduction in cavity area observed by bright field microscopy of tissues, that is, from 1 to 10 and from 0.20 ± 0.05 mm(2) to 0.10 ± 0.03 mm(2), in Sal B treated group, respectively, compared to PBS group. Statistical analysis was carried out using SPSS software (SPSS, Chicago, IL, USA), values were expressed as mean ± SEM, and P value <0.01 was considered significant. Effect of Sal B on expression of NF-kB p65 and IkB α was studied and OD values of densitometry of western blots were taken. MPO activity was also studied. It was observed that treatment of Sal B significantly reduced the expression of both compounds in Sal B treated group as compared to control group after 28 days of treatment.


Subject(s)
Caffeic Acids/pharmacology , Lactates/pharmacology , Motor Activity/drug effects , Proton Pump Inhibitors/pharmacology , Spinal Cord Injuries , Animals , Female , I-kappa B Proteins/metabolism , NF-KappaB Inhibitor alpha , Nerve Tissue Proteins/metabolism , Rats , Rats, Sprague-Dawley , Spinal Cord Injuries/drug therapy , Spinal Cord Injuries/metabolism , Spinal Cord Injuries/pathology , Spinal Cord Injuries/physiopathology , Time Factors , Transcription Factor RelA/metabolism
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