scholarly journals PROTEOMIC DATASET: Profiling of glioma C6 and astrocytes rat cell lines before and after co-cultivation.

Data in Brief ◽  
2021 ◽  
pp. 107658
Author(s):  
Artemiy S. Silantyev ◽  
Olga N. Bukato ◽  
Ivan O. Butenko ◽  
Anastasia A. Chernysheva ◽  
Olga V. Pobeguts ◽  
...  
Keyword(s):  
Cell Lines ◽  
Glioma C6 ◽  
Before And After ◽  
Proteomic Dataset

MiR-597 Targeting 14-3-3σ Enhances Cellular Invasion and EMT in Nasopharyngeal Carcinoma Cells

2019 ◽  
Vol 12 (2) ◽  
pp. 105-114 ◽  
Author(s):  
Lisha Xie ◽  
Tao Jiang ◽  
Ailan Cheng ◽  
Ting Zhang ◽  
Pin Huang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Cell Lines ◽  
Western Blotting ◽  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Suppressor Gene ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Downstream Target ◽  
Before And After

Background: Alterations in microRNAs (miRNAs) are related to the occurrence of nasopharyngeal carcinoma (NPC) and play an important role in the molecular mechanism of NPC. Our previous studies show low expression of 14-3-3σ (SFN) is related to the metastasis and differentiation of NPC, but the underlying molecular mechanisms remain unclear. Methods: Through bioinformatics analysis, we find miR-597 is the preferred target miRNA of 14-3-3σ. The expression level of 14-3-3σ in NPC cell lines was detected by Western blotting. The expression of miR-597 in NPC cell lines was detected by qRT-PCR. We transfected miR-597 mimic, miR-597 inhibitor and 14-3-3σ siRNA into 6-10B cells and then verified the expression of 14-3-3σ and EMT related proteins, including E-cadherin, N-cadherin and Vimentin by western blotting. The changes of migration and invasion ability of NPC cell lines before and after transfected were determined by wound healing assay and Transwell assay. Results: miR-597 expression was upregulated in NPC cell lines and repaired in related NPC cell lines, which exhibit a potent tumor-forming effect. After inhibiting the miR-597 expression, its effect on NPC cell line was obviously decreased. Moreover, 14-3-3σ acts as a tumor suppressor gene and its expression in NPC cell lines is negatively correlated with miR-597. Here 14-3-3σ was identified as a downstream target gene of miR-597, and its downregulation by miR-597 drives epithelial-mesenchymal transition (EMT) and promotes the migration and invasion of NPC. Conclusion: Based on these findings, our study will provide theoretical and experimental evidences for molecular targeted therapy of NPC.

Different drug sensitivity in two neuroblastoma cell lines established from the same patient before and after chemotherapy

1991 ◽  
Vol 47 (5) ◽  
pp. 732-737 ◽  
Author(s):  
Hiroshi Kuroda ◽  
Tohru Sugimoto ◽  
Kazumitsu Ueda ◽  
Shigeki Tsuchida ◽  
Yoshihiro Horii ◽  
...  
Keyword(s):  
Cell Lines ◽  
Drug Sensitivity ◽  
Neuroblastoma Cell ◽  
Before And After ◽  
Neuroblastoma Cell Lines

PROTEOMIC ANALYSIS OF ASTROCYTE CELL LINE BEFORE AND AFTER CO-COCULTIVATION WITH RATTUS NORVEGICUS GLIOMA C6 CELLS

2020 ◽  
pp. 174-176
Author(s):  
A. Chernysheva ◽  
O. Pobeguts ◽  
A. Nosyrev ◽  
G. Pavlova ◽  
O. Gurina
Keyword(s):  
Cell Line ◽  
Proteomic Analysis ◽  
Glioma Cells ◽  
Glioma Cell Line ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Glioma C6 ◽  
Before And After ◽  
Normal Rat ◽  
Rat Astrocytes

We perfomed panoramic proteomic analysis of rat C6 glioma cells, native rat astrocytes and rat astrocytes co- cultivated with C6 glioma cell line. Based on the data, a putative model was present for the diagnostic differentiation of normal rat astrocytes from C6 glioma cells.

scholarly journals Comparison of BGM and PLC/PRC/5 Cell Lines for Total Culturable Viral Assay of Treated Sewage

2008 ◽  
Vol 74 (9) ◽  
pp. 2583-2587 ◽  
Author(s):  
Roberto A. Rodríguez ◽  
Patricia M. Gundy ◽  
Charles P. Gerba
Keyword(s):  
Activated Sludge ◽  
Cell Lines ◽  
Uv Light ◽  
Treatment Plant ◽  
High Rate ◽  
Uv Treatment ◽  
Cell Monolayers ◽  
Reverse Transcription Pcr ◽  
Treated Sewage ◽  
Before And After

ABSTRACT The objective of this study was to compare PLC/PRF/5 and BGM cell lines for use in a total culturable viral assay (TCVA) of treated sewage effluents. Samples were collected before and after chlorination from an activated sludge wastewater treatment plant and from the effluent of a high-rate enhanced flocculation system, followed by UV light disinfection. Cell monolayers were observed for cytopathic effect (CPE) after two passages of 14 days each. Monolayers exhibiting viral CPE were tested for the presence of adenoviruses and enteroviruses by PCR or reverse transcription-PCR. Eight percent of the samples exhibited CPE on BGM cells, and 57% showed CPE on PLC/PRF/5 cells. Only enteroviruses were detected on the BGM cells, while 30% and 52% of the samples were positive for enteroviruses and adenoviruses, respectively, on the PLC/PRF/5 cells. Thirty percent of the samples were positive for both adenoviruses and enteroviruses in chlorinated activated sludge effluent. Thirty percent of the samples were positive for adenoviruses in the UV treatment effluent, but no enteroviruses were detected. In conclusion, the PLC/PRF/5 cells were more susceptible than BGM cells to viruses found in treated sewage. The use of BGM cells for TCVA may underestimate viral concentration in sewage effluent samples. The PLC/PRF/5 cells were more susceptible to adenoviruses, which is important in the evaluation of UV disinfection systems because adenoviruses are highly resistant to UV inactivation.

Constitutive FLT3 Activation Results in Specific Changes in Gene Expression in Myeloid Leukemic Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1115-1115
Author(s):  
Kyu-Tae Kim ◽  
Kristin Baird ◽  
Sean Davis ◽  
Mark Levis ◽  
Obdulio Piloto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Microarray Analysis ◽  
Cdna Microarray ◽  
Mapk Pathway ◽  
Cyclin D3 ◽  
Leukemic Cells ◽  
Cdna Microarray Analysis ◽  
Flt3 Inhibitors ◽  
Before And After

Abstract Constitutively activating internal tandem duplication (ITD) mutations of the receptor tyrosine kinase FLT3 play an important role in leukemogenesis. They are the most common genetic alteration in AML and their presence is associated with poor prognosis. To better understand FLT3 signaling in leukemogenesis, we have examined the changes in gene expression induced by FLT3/ITD or constitutively activated wild type FLT3 signaling by cDNA microarray analysis. In order to minimize gene expression changes that might be drug specific and not related to FLT3 inhibition or might be cell-type specific, we used three different FLT3 inhibitors, CEP-701, CEP-5214, and AG1296, and three different constitutively activated FLT3-expressing leukemia-derived cell lines, EOL-1, MOLM-14 and MV4-11. We considered to be FLT3 responsive only those genes whose expression consistently changed in response to FLT3 inhibition by each of the three FLT3 inhibitors in all of the cell lines. RNA for hybridization to the microarrays was harvested from cells both before and after increasing times of FLT3 inhibition to determine genes which decreased or increased in response to FLT3 signaling. In addition, because the inhibitors are all reversible, RNA was also harvested from the cells at increasing times after release from FLT3 inhibition. This enabled us to confirm that, for example, genes whose expression appeared FLT3 dependent and were thus down-regulated by FLT3 inhibition, returned towards normal levels after FLT3 signaling was allowed to resume. Statistical analysis of the microarray results indicated a limited set of genes are highly and consistently affected by FLT3 inhibition and return toward pretreatment levels after release from inhibitor. We confirmed the cDNA microarray data using quantitative real-time PCR. Several of the most significantly affected genes are involved in the Ras/MAPK pathway including DUSP6, DUSP7, MAPK6, TNF, and cMyc. Other sets of genes are involved in JAK/STAT or Wnt signaling pathways including Pim-1, cMyc, Cyclin D3, IL4 receptor, and CISH. These genes are all consistently down-regulated after FLT3 inhibition. These data further confirm the role of constitutively activating FLT3 in mediating multiple signal transduction pathways. We also found several transcriptional factors (RUNX1/AML1, MAFG, XBP1, TGFBI4, and BRD8), several genes involved in receptor-mediated signaling (IL1RAP, CDC42EP3, PLAUR, LY64), and several genes involved in cell proliferation, metabolism, or structure (BCL7A, APTX, GHRH, SET7, ATAD2, CLIC1, CRIP2, MRPL12, VIM) to be consistently differentially expressed. In summary, we have found by cDNA microarray analysis and confirmed by QPCR, a consistent pattern of FLT3 dependent gene expression. The alteration of the gene expression profile in these cells is likely the mechanism of FLT3-mediated leukemogenisis.

Effects of rmhTRAIL Combined with Daunorubicin in Inducing Apoptosis of Leukemia Cell Lines and Its Mechanism.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1986-1986
Author(s):  
Xuejun Zhang ◽  
Li Wen ◽  
Fuxu Wang ◽  
Ling Pan ◽  
Jianmin Luo ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Cell Line ◽  
Cell Lines ◽  
Mrna Level ◽  
Leukemia Cell ◽  
K562 Cells ◽  
Expression Level ◽  
U937 Cells ◽  
Leukemia Cell Lines ◽  
Before And After

Abstract Tumor Necrosis factor (TNF)-related apoptosis- inducing ligand (TRAIL) is a new member of TNF superfamily discovered recently. Several studies showed that TRAIL can preferentially induce apoptosis in a variety of tumor cells, while most normal cells tested do not appear to be sensitive to TRAIL. In the present study, we treated K562 and U937 leukemia cell lines with recombinant mutant human TRAIL (rmhTRAIL) alone or together with daunorubicin (DNR) to investigate the apoptosis of the treated cells and the synergistic reaction of rmhTRAIL and DNR. The normal cell line MRC-5 was used as control. The expression of four TRAIL receptors mRNA (death receptor DR4 and DR5, decoy receptor DcR1 and DcR2) in the cells lines were detected before and after the treatment by DNR. (1) AO-EB double staining and TUNEL staining were used to evaluate the morphological change of leukemia cell lines before and after the treatment. The results showed that rmhTRAIL could induce the apoptosis of leukemia cell lines and a dose-dependent manner was found in leukemia cell lines but not in MRC-5 cell lines. (2) The growth inhibition rate of leukemia cell lines induced by rmhTRAIL alone or combined with DNR was examined with MTT assays. Different concentrations of rmhTRAIL(8, 40, 200, 1000ng/mL)alone or combined with DNR(8, 40, 200, 1000ng/mL) was used. The result showed a dose-dependent growth inhibition by rmhTRAIL alone for K562- and U937-cell line (P<0.05) also, but not for MRC-5 cell line (P>0.05). The IC50 for K562 cells and for U937 cells had no statistic difference (538.80 vs 301.56ng/mL, P>0.05). In leukemia cell lines, the growth inhibition rates in combination groups were much higher than in rmhTRAIL or DNR alone groups (P<0.05), and no synergistic killing effects was found in MRC-5 cells (P<0.05). It was concluded that rmhTRAIL had synergistic effects with DNR in the growth inhibition of K562 and U937 cells. (3). To explore the antitumor mechanisms of rmhTRAIL combined with DNR, the expression level of the DR4, DR5 and DcR1, DcR2 mRNA in these three cell lines was examined by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) before and after the treatment with DNR. The high expression of DR4,DR5 mRNA in the tested cells were observed before the treatment of DNR, while very low or even undetectable expression level of DcR1 and DcR2 mRNA were observed in U937 and K562 cells, and a high expression level of DcR1 and DcR2 mRNA in MRC-5 cells were observed. After 24 hours treatment of three cell lines with DNR (200ng/ml), the expression level of DR5 mRNA increased in K562 and U937 cells (P<0.05). DR4 mRNA also increased in K562 cells but not in U937 cells. There was no change in DcR1 and DcR2 mRNA level in three cell lines. The four receptors’ mRNA level in MRC-5 cells was not influenced by DNR. Our results indicated that rmhTRAIL could induce the apoptosis of leukemia cell lines, and DNR could enhance significantly the sensitivity of K562 and U937 cells to apoptosis induced by rmhTRAIL through up-regulation of death receptors. Therefore, we presumed TRAIL might be act as a new agent for biological therapy in leukemia.

Transiently Elevated AST/LDH Are Associated with Clinical Response to Recombinant Circularly Permuted TRAIL (CPT) Plus Thalidomide in Patients with Relapsed and/or Refractory Multiple Myeloma

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 3478-3478
Author(s):  
Wenming Chen ◽  
Peng Wei ◽  
Shifang Yang ◽  
Xiangjun Zheng ◽  
Lugui Qiu ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Death ◽  
Cell Lines ◽  
Time Course ◽  
Single Agent ◽  
Release Rates ◽  
Refractory Multiple Myeloma ◽  
Before And After ◽  
Clinical Responses ◽  
Thalidomide Treatment

Abstract Introduction: Circularly permuted TRAIL (CPT), a recombinant mutant of human Apo2L/TRAIL, is a promising anti-tumor candidate. In previous phase1/2 clinical trials of single-agent CPT in patients with relapsed and/or refractory multiple myeloma (RRMM), transient elevations of serum AST and LDH were observed early after CPT treatment in most response patients, but not in the non-respondent. Positive correlations were found between increased AST/LDH on day 2 or 3 (24 or 48 hours) after CPT initial dosing and the clinical responses to CPT. Objective: To determine whether transiently elevated AST/LDH is predictive of responses to CPT plus thalidomide in thalidomide-relapsed or refractory MM patient and the time course of AST or LDH elevation. Methods: We retrospectively analyzed the data of a phase 2 study of CPT plus thalidomide. The changes of serum AST, LDH or ALT were analyzed before treatment and on days 2, 3 and 6 after initial dosing. Relationship was evaluated between ΔAST, ΔLDH, ΔALT (ratio of ASTD2, LDHD2 or ALTD2to baseline value) and the best clinical responses. Four MM cell lines (RPMI 8226, NCI-H929, MM.1S, MM.1R) sensitive to CPT were used to detect the concentrations of AST, ALT and LDH in the cytoplasm or the medium of CPT-treated cells, with the purpose of determining whether CPT-induced cell death could result in an elevation of AST or LDH. Results: Of 41 efficacy-evaluable patients, 9(22.0%) achieved a partial response (PR) or better and 14 (34.1%) achieved a minimal response (MR) or better. The serum ASTD2 and LDHD2 levels were dramatically increased from baseline in patients with ≥PR or ≥MR, but not in those with NC/PD. However, serum ALTD2 was comparable to baseline value either in response patients (≥PR or ≥MR) or in non-response ones (NC/PD). Consequently, the median ΔAST or ΔLDH of patients with ≥PR or ≥MR was significantly higher than that of patients with NC/PD (Table 1). The elevation of AST or LDH was transient with a peak on day 2 after treatment, then dramatically declined on day 3, and usually disappeared within one week (at most two weeks for LDH) (Figure 1), which was uniquely observed in the first treatment cycle. A univariate logistic-regression analysis showed that ΔASTwas predictive of achieving responses of ≥MR or not (P=0.04). Indeed, patients with higher level of ΔAST had higher probability of achieving responses of ≥MR (72.7% in patients with ΔAST>1.35 vs. 26.3% in patients with ΔAST≤1.35). In the cytoplasm of MM cell lines, abundant AST and LDH but only detectable level of ALT was observed. There was no significant change in the release rates of AST and LDH with CPT incubation for 1, 2, 3, 4 or 6 hours, even though the cell viabilities at 6h had already declined to about 10-20% of the control cells by ATP chemiluminescent assay. Remarkable increase in the release rates of AST and LDH occurred at 24h, with no evident change of ALT, which was consistent with what was observed in patients in the clinical study. It was suggested that the transient elevation of AST or LDH in RRMM patients was most likely resulted from CPT-induced myeloma cell death. Conclusion: The early transient elevations of serum AST and LDH after CPT plus thalidomide treatment were positively correlated with the clinical responses to CPT plus thalidomide, and were possibly resulted from CPT-induced cell death. ΔAST on day2 could be a surrogate response biomarker for CPT treatment in RRMM patients. Figure 1 Representative time course of AST, ALT or LDH changes before and after CPT plus thalidomide treatment in response patients Figure 1. Representative time course of AST, ALT or LDH changes before and after CPT plus thalidomide treatment in response patients Table 1 Differences in ΔAST, ΔALT and ΔLDH between response patients (≥PR or ≥MR) and non-response patients (NC/PD) Table 1. Differences in ΔAST, ΔALT and ΔLDH between response patients (≥PR or ≥MR) and non-response patients (NC/PD) Disclosures Wei: Beijing Sunbio Biotech Co., Ltd.: Employment. Yang:Beijing Sunbio Biotech Co., Ltd.: Employment. Zheng:Beijing Sunbio Biotech Co., Ltd.: Employment. Pang:Beijing Sunbio Biotech Co., Ltd.: Employment.

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