scholarly journals Antisense oligonucleotide p45Skp-2 suppresses migratory chemotactic and metastasis of oral malignant Burkitt’s lymphoma cell through down-regulation of MTA-1 and induction of E-cadherin mechanism

2020 ◽  
Vol 32 (3) ◽  
pp. 220
Author(s):  
Supriatno Supriatno ◽  
Dyah Irnawati ◽  
Ana Medawati
Keyword(s):  
Internal Control ◽  
Raji Cell ◽  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Control Group ◽  
Boyden Chamber ◽  
Chemotactic Migration ◽  
Down Regulation ◽  
Tubulin Protein ◽  
E Cadherin

Introduction: Burkitt’s lymphoma is a high-grade B-cell neoplasm and one of the most aggressive malignancies of lymphoid origins which found mainly in the paediatric population. The treatment options of this tumour are still limited. However, a new strategy for refractory tumour, phosphorothioate oligonucleotide antisense technique has watched with keen interest. This study was aimed to examine the effect of antisense p45Skp-2 (Skp-2 AS) suppressed migratory chemotactic and metastasis of oral malignant Burkitt’s lymphoma (Raji) cell through down-regulation of MTA-1 and E-cadherin. Methods: True experiment laboratory with post-test control group design was confirmed in this study. The efficiency of Skp-2 AS in the suppression of cell chemotactic migration was examined by Boyden chamber assay. To evaluate the inhibition of cell metastasis was conducted by decreasing MTA-1 expression protein. The expressions of MTA-1, E-cadherin and α-tubulin protein were investigated by Western blot analysis. Results: The results revealed that the number of chemotactic migration of Skp-2 AS treated Raji cell was significantly decreased when compared with that of sense p45Skp-2 (Skp-2 S) and scrambled control (SC) cells (P<0.05) followed by decreased expressions of MTA-1 protein and overexpression of E-cadherin. Interestingly, the expression of α-tubulin protein as an internal control was approximately similar in each transfectant cells. Conclusion: p45Skp-2 have an antitumor activity via suppression of migratory chemotactic activity and metastasis on oral Burkitt’s lymphoma cells through down-regulation of MTA-1 and induction of E-cadherin proteins targeting this molecule could represent a promising new therapeutic approach for this type of cancer.

Anti-Tumor Effect of a Novel DOX/GA-CdTe QD was Mediated by Apoptotic and Autophagic Cell Death

NANO ◽  
2017 ◽  
Vol 12 (01) ◽  
pp. 1750011 ◽  
Author(s):  
Huaqin Zuo ◽  
Fan Wang ◽  
Di Zhou ◽  
Yi Zhou ◽  
Bing Chen ◽  
...  
Keyword(s):  
Cell Line ◽  
Raji Cell ◽  
Combined Treatment ◽  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Gambogic Acid ◽  
Myc Oncogene ◽  
Cdte Qds ◽  
M Phase ◽  
Relapsed Disease

Burkitt’s lymphoma is a highly proliferative B-cell malignancy characterized by MYC oncogene translocation. Intensive short-cycle chemotherapy could effectively improve the outcome of this disease. However, drug resistance limits the treatment of refractory/relapsed disease. Thus, we constructed and investigated a novel cadmium–tellurium quantum dot conjugated with doxorubicin and gambogic acid (DOX/GA-CdTe QDs) for cancer cell combined treatment in Raji, a Burkitt’s lymphoma cell line. Results showed that DOX/GA-CdTe QDs could significantly improve anti-tumor effects compared with drugs alone in the Raji cell line. Flow cytometry, transmission electron micrographs and overexpression of Beclin1 and LC3 II/I showed that apoptosis and autophagy were involved in the process. However, DOX/GA-CdTe QDs did not cause cell cycle arrest, whereas DOX alone or combined with GA could cause apparent G2/M phase arrest. Hence, the novel DOX/GA-CdTe QDs offer a promising approach of drug delivery into cancer cells.

The Epstein-Barr Virus (EBV) Encoded Oncoprotein LMP1 Mediates Down Regulation of Shelterin Proteins, Formation of Telomere Aggregates and Multinuclearity.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3625-3625
Author(s):  
Valérie Lajoie ◽  
Bruno Lemieux ◽  
Bassem Sawan ◽  
Daniel Lichtensztejn ◽  
Zelda Lichtensztejn ◽  
...  
Keyword(s):  
Hodgkin’S Lymphoma ◽  
Burkitt’S Lymphoma ◽  
Tumour Cells ◽  
Nuclear Volume ◽  
Burkitt's Lymphoma ◽  
Hodgkin's Lymphoma ◽  
Down Regulation ◽  
Lmp1 Expression ◽  
Increased Risk ◽  
Telomere Dynamics

Abstract Abstract 3625 Introduction: Tumour cells in classical Hodgkin's lymphoma (HL) and Burkitt's lymphoma (BL) are derived from germinal center B-cells and may or may not harbour the EBV genome. In both, EBV-negative and EBV-associated HL, the 3D nuclear organization of telomeres marks the transition from mononuclear Hodgkin (H-cell) to diagnostic multinuclear Reed-Sternberg (RS-cell) cells. Moreover, transient expression of the EBV-encoded oncoprotein LMP1 in the HL cell lines L-428 and HD-MyZ significantly increases the percentage of RS cells. However, the molecular mechanisms through which this selective LMP1 oncoprotein expression promotes the transition from H- to RS-cells is still unknown. In order to answer this question we analyzed the 3D telomere dynamics and the expression of key shelterin proteins at the transcriptional, translational and topographical localization level in the EBV-negative Burkitt cell line BJAB, stably transfected with an inducible LMP1 system (tetracycline on/off system). To mimic the permanent LMP1 expression as observed in tumour cells of EBV-associated Hodgkin's lymphoma, we extended the period of LMP1 expression up to 21 days and examined key proteins of the shelterin complex, 3D telomere dynamics and formation of multinuclear cells in interphase nuclei of BJAB Burkitt's lymphoma cells at day 1, 3, 7, 10, 14 and 21. Statistical analysis was performed using nested or two-way analysis of variance. Results: Already at day 3 LMP1 induced substantial down regulation of the shelterin key-components TRF1, TRF2 and POT1 at the transcriptional and protein level. This down regulation was reversible after LMP1 suppression; in particular, suppression of LMP1 induction at day 7 returned shelterin-key components to the initial level of expression at day 14. Massive LMP1 mediated down regulation of shelterin proteins was also confirmed by immunofluorescence. At day 7, stable LMP1 expression led to a significant increase of 3D telomere aggregates, nuclear volume and polyploid cells, most of them multinucleated, when compared to non-LMP1 expressing BJAB controls (p < 0.02). These changes progressed over time and at day 21 LMP1 expressing BJAB cells were characterized by highly significant increase of 3D telomere aggregates (p = 0.0005) and increased nuclear volume (p < 0.0001), compared to the LMP1-suppressed control. Discussion: In an experimental setting mimicking the in vivo conditions of EBV-associated HL, i.e. a permanent LMP1 expression in the H-cells, the LMP1 oncoprotein deregulates shelterin-expression, leads to telomere aggregates and mediates multinuclearity. Our findings point to a shelterin/telomere related key function of LMP1 in Reed-Sternberg cell formation in EBV-associated Hodgkin's lymphoma and may explain the four fold increased risk to develop HL within a median incubation time of four years after symptomatic EBV infection. The LMP1-dependent mechanisms involved are probably unprotected telomeres (shelterin down regulation) favouring chromosomal rearrangements as a result of telomeric aggregate formation and ongoing bridge-fusion- bridge cycles which lead to disturbed cytokinesis and finally multinuclearity. Disclosures: No relevant conflicts of interest to declare.

Etodolac Inhibits EBER Expression and Induces Bcl-2-Regulated Apoptosis in Burkitt’s Lymphoma Cells.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4825-4825
Author(s):  
Miki Kobayashi ◽  
Satoki Nakamura ◽  
Kiyoshi Shibata ◽  
Naohi Sahara ◽  
Kazuyuki Shigeno ◽  
...  
Keyword(s):  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Lymphoma Cells ◽  
Down Regulation ◽  
Raji Cells ◽  
Protein Activation ◽  
Cox 2 ◽  
Induced Apoptosis ◽  
Cox 2 Inhibitors ◽  
Burkitt’S Lymphoma Cells

Abstract Cyclooxygenase-2 (COX-2) is reported to be an important cellular target for therapy in malignancies. The growth inhibitory effects of COX-2 inhibitors on malignancies have been demonstrated to be through not only COX-2 dependent, but also independent mechanisms. In this study, we showed that etodolac, COX-2 inhibitor, induced apoptosis via COX-2 independent pathway, and investigated the molecular details of etodolac-induced apoptosis in Burkitt’s lymphoma cells. In Daudi and Raji Burkitt’s lymphoma cell lines, which expressed no COX-2 enzyme, etodolac more strongly induced apoptosis compared to meloxicam. Moreover, Etodolac did not induce apoptosis to normal B lymphocytes. For the pathway of etodolac-induced apoptosis, reduction of anti-apoptotic bcl-2 mRNA and Bcl-2 protein, activation of Caspase-9 and -3, down-regulation of caspase inhibitors, c-IAP-1 and Survivin were involved. Moreover, EBER-1 and -2 expression in EBV positive Daudi and Raji cells were reduced to result in down-regulation of Bcl-2 by treatment with etodolac. It has been reported that etodolac has stereoisomers, R- and S- etodolac. We found that racemate of etodolac more strongly induced apoptosis in Daudi and Raji cells compared to R- or S- etodolac. In conclusion, our findings indicated etodolac inhibited EBERs expression and induced apoptosis via a Bcl-2-regulated pathway. Moreover, racemate of etodolac more effectively induced apoptosis than R- and/or S- etodolac. Therefore, these activities of etodolac potentially extend to the treatment of patients with Burkitt’s lymphoma resistant to chemotherapy.

scholarly journals CD95-mediated apoptosis in Burkitt's lymphoma B-cells is associated with Pim-1 down-regulation

2017 ◽  
Vol 1863 (1) ◽  
pp. 239-252 ◽  
Author(s):  
Sabine Matou-Nasri ◽  
Zaki Rabhan ◽  
Haya Al-Baijan ◽  
Hamad Al-Eidi ◽  
Wesam Bin Yahya ◽  
...  
Keyword(s):  
B Cells ◽  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Down Regulation

Mechanisms of allele-selective down-regulation of HLA class I in Burkitt's lymphoma

1995 ◽  
Vol 62 (1) ◽  
pp. 90-96 ◽  
Author(s):  
Marta P. Imreh ◽  
Qian-Jin Zhang ◽  
Pedro O. De Campos-Lima ◽  
Stephan Imreh ◽  
Peter Krausa ◽  
...  
Keyword(s):  
Hla Class I ◽  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Class I ◽  
Down Regulation

scholarly journals E-cadherin, Snail, ZEB-1, DNMT1, DNMT3A and DNMT3B expression in normal and breast cancer tissues*

2019 ◽  
Author(s):  
Shaian Tavakolian ◽  
Hossein Goudarzi ◽  
Ebrahim Faghihloo
Keyword(s):  
Breast Cancer ◽  
Dna Methyltransferase ◽  
Dna Methyltransferases ◽  
Control Group ◽  
Down Regulation ◽  
Expression Levels ◽  
Normal Tissues ◽  
Cancer Pathogenesis ◽  
Cancer Tissues ◽  
E Cadherin

Objective: Breast cancer is known as one of very important cancers among females, given that a variety of external (i.e., environmental risk factors) and internal factors (i.e., genetics, and epigenetics) are related to the emergence and progression of breast cancer. Among genetic and epigenetic factors, DNA methyltransferase and EMT related genes have critical roles in breast cancer pathogenesis. In the study presented here, we investigated expression of DNA methyltransferases (e.g., DNMT1, DNMT3A and DNMT3B) and EMT related genes (e.g., E-cadherin, Snail, ZEB-1). Methods and Materials: Tissue samples were collected from 18 cancer and 24 normal breast tissues. We evaluated the expression levels of DNA methyltransferases and EMT related genes using Quantitative real-time PCR (qRT-PCR). Results: Our results indicated that the expression levels of ZEB-1, Snail, and DNMT3B were increased in breast cancer subjects in comparison to the control group. On the other hand, there was a significant decrease in E-cadherin expression in breast cancer tissues in comparison to the normal tissues. Moreover, there were no significant changes for DNMT1 and DNMT3A expression in breast cancer tissues when compared to the normal tissues. Conclusion: Taken together, our finding show that up regulation of ZEB-1 and Snail could be associated with down regulation of E-cadherin and results in promotion of cancer cell invasion. Moreover, down regulation of E-cadherin may be related to deterioration of DNMT3B inpatients with breast cancer.

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