scholarly journals MicroRNA-15a modulates lens epithelial cells apoptosis and proliferation through targeting B-cell lymphoma-2 and E2F transcription factor 3 in age-related cataracts

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Qiao Li ◽  
HaiTao Pan ◽  
QingHuai Liu
Keyword(s):  
Cell Proliferation ◽  
Transcription Factor ◽  
B Cell ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Age Related ◽  
E2f Transcription Factor

Abstract Age-related cataract remains a serious problem in the aged over the world. MicroRNAs are abnormally expressed in various diseases including age-related cataract. MicroRNA-15a (MicroRNA-15a) has been involved in various diseases and plays crucial roles in many cellular processes. However, the mechanism of microRNA-15a in the genesis of cataract remains barely known. We therefore aimed to investigate the role of microRNA-15a in the cataract. Herein, human lens epithelial B3 cells, HLE-B3 cells were treated with 200 μmol/l H2O2 for 24 h. H2O2 was utilized in our study to induce HLE-B3 cells injury. We observed that cell apoptosis was induced by the treatment of H2O2 and meanwhile, cell proliferation was repressed by 200 μmol/l H2O2. Then, it was found that microRNA-15a was significantly increased with the H2O2 exposure in vitro. Importantly, B-cell lymphoma-2 (BCL2) and E2F transcription factor 3 (E2F3) exert crucial roles in cell apoptosis and cell proliferation. We found that BCL2 and E2F3 were greatly reduced by 200 μmol/l H2O2 in human lens epithelial cells. In addition, microRNA-15a overexpression induced cell apoptosis and repressed cell proliferation through suppressing BCL2 and E2F3. Subsequently, BCL2 and E2F3 were predicted as a direct target of microRNA-15a. The direct correlation between microRNA-15a and BCL2/E2F3 was confirmed by dual luciferase reporter assay. In conclusion, we demonstrated that microRNA-15a triggered apoptosis and repressed the proliferation of HLE-B3 cells by modulating BCL2 and E2F3.

LINC00857 contributes to proliferation and lymphomagenesis by regulating miR-370-3p/CBX3 axis in diffuse large B cell lymphoma

2021 ◽  
Author(s):  
Yan Huang ◽  
Yuanyuan Lin ◽  
Xiangxiang Song ◽  
Depei Wu
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
Ectopic Expression ◽  
B Cell Lymphoma ◽  
Nuclear Antigen ◽  
Large B Cell Lymphoma ◽  
The Impact ◽  
Large B Cell

Abstract Diffuse large B-cell lymphoma (DLBCL) remains to be a high aggressive and invasive malignancy with enigmatic etiology. Ectopic expression of long noncoding RNAs are widely involved in the progression of human cancers. We discovered that LINC00857 level was remarkably elevated in DLBCL tissues compared with non-tumor controls. High LINC00857 level predicts lower survival rate, more advanced tumor node metastasis and larger tumor size. LINC00857 overexpression promoted DLBCL cell proliferation and facilitated cell cycle as evidenced by elevated cyclinD1 and proliferating cell nuclear antigen (PCNA) accompanying with reduced p21 level. LINC00857 overexpression also suppressed DLBCL cell apoptosis as evidenced by elevated Bcl-2 protein level, reduced Bax and cleaved caspase-3 protein levels. On the contrary, LINC00857 knockdown using short hairpin RNAs inhibited DLBCL cell proliferation yet induced cell apoptosis. LINC00857 knockdown also repressed tumor growth in vivo, concomitant with decreased Ki67 level. Besides, microRNA miR-370 was down-regulated in DLBCL tissues and served as a competitive endogenous RNA (ceRNA) target of LINC00857. We further validated that chromobox homolog 3 (CBX3) served as a downstream target gene of miR-370-3p. LINC00857 level was reversely correlated with miR-370-3p level yet positively correlated with CBX3 level. In addition, CBX3 overexpression alleviated the impact of LINC00857 knockdown on DLBCL cell survival. In conclusion, our findings indicated that LINC00857 contributes to DLBCL proliferation and lymphomagenesis through regulating miR-370-3p/CBX3 axis.

scholarly journals LncRNA SNHG8 Promotes Proliferation and Inhibits Apoptosis of Diffuse Large B-Cell Lymphoma via Sponging miR-335-5p

2021 ◽  
Vol 11 ◽  
Author(s):  
Bing Yu ◽  
Bo Wang ◽  
Zhuman Wu ◽  
Chengnian Wu ◽  
Juan Ling ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Cell Apoptosis ◽  
Colony Formation ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Luciferase Assay ◽  
Promoting Effect ◽  
Large B Cell Lymphoma ◽  
Large B Cell

Long-chain non-coding RNAs (LncRNAs) are expressed in diffuse large B-cell lymphoma (DLBCL) tissues and have played a regulatory role in DLBCL with a cancer-promoting effect. In this study, the role of LncRNA SNHG8 in the regulation of DLBCL cells is investigated, and its underlying mechanism is explored. The database of the Gene Expression Profiling Interactive Analysis (GEPIA) was searched, and the expression of SNHG8 in DLBCL and normal tissues was examined. The expression of SNHG8 was evaluated in several DLBCL cell lines and a normal lymphocyte cell line. It was found that SNHG8 was overexpressed in DLBCL tissues and cells in comparison with their normal counterparts. The short hairpin RNA (shRNA) plasmids of SNHG8 were transfected into DLBCL cells to knockdown the expression of SNHG8, followed by assays of proliferation, colony formation, apoptosis, and related protein expression. The results showed that the knockdown of SNHG8 significantly inhibited DLBCL cell proliferation and colony formation while promoting cell apoptosis. Moreover, the knockdown of SNHG8 reduced the expression of Ki-67, proliferating cell nuclear antigen (PCNA), and Bcl-2 and enhanced the expression of Bax and cleaved caspase 3/9. MiR-335-5p was predicted to be a potential target of SNHG8 by using the bioinformatics analysis, and the interaction between the two was validated by using the dual luciferase assay. In addition, the knockdown of SNHG8 increased the level of miR-335-5p, whereas miR-335-5p mimic decreased the expression of SNHG8. Finally, U2932 cells were co-transfected with or without sh-SNHG8 and miR-335-5p inhibitors, whose proliferation, colony formation, and apoptosis were determined subsequently. It was demonstrated that the presence of an miR-335-5p inhibitor partially canceled the inhibitory effects of the knockdown of SNHG8 on DLBCL cell proliferation and colony formation and the stimulating effects of the knockdown of SNHG8 on cell apoptosis. Taken together, our study suggests that lncRNA SNHG8 exerts a cancer-promoting effect on DLBCL via targeting miR-335-5p.

scholarly journals miR-10a inhibits cell proliferation and promotes cell apoptosis by targeting BCL6 in diffuse large B-cell lymphoma

2016 ◽  
Vol 7 (12) ◽  
pp. 899-912 ◽  
Author(s):  
Qian Fan ◽  
Xiangrui Meng ◽  
Hongwei Liang ◽  
Huilai Zhang ◽  
Xianming Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Large B Cell Lymphoma ◽  
Large B Cell

miR-4262 Targets Anti-Apoptotic Gene B-Cell Lymphoma-2 to Induce Cell Apoptosis and Inhibit Cell Proliferation in Oral Squamous Cell Carcinoma

2020 ◽  
Vol 10 (6) ◽  
pp. 804-811
Author(s):  
Guangyao Hu ◽  
Dianxiu Wu
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Viability ◽  
B Cell ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Luciferase Reporter ◽  
Qrt Pcr

Oral squamous cell carcinoma (OSCC), a frequently happened cancer, is still an important threaten to human with unsatisfactory prognosis. Increasing evidence indicated that abnormal miRNA expressions were related to the development of OSCC. microRNA (miR)-4262 has been considered to be a cancer suppressor in various tumors, however its exact role in OSCC remains to be clarified. During the current research, we proposed to probe the biological activity and fundamental mechanism of miR-4262 in OSCC. The expression levels of miR-4262 in SCC9 and HOK cells were analyzed using quantitative real time polymerase chain reaction (qRT-PCR). TargetScan and luciferase reporter assay were carried out to quest the possible target gene of miR-4262. qRT-PCR and Western blotting analysis were employed to measure the expressions of B-cell lymphoma-2 (Bcl-2) in OSCC tissues, adjacent non-cancerous tissues, SCC9 and HOK cells. Cell proliferation and apoptosis of SCC9 cells were detected by Thiazolyl Blue Tetrazolium Bromide (MTT) and flow cytometry (FCM) analysis. The expressions of apoptosis-related proteins Bcl-2 and Bcl2-associated X protein (Bax) were checked by Western blotting analysis. Firstly, we found that miR-4262 expressed lower level in OSCC cells than that in the control. Results from TargetScan and luciferase reporter analysis showed that miR-4262 directly targeted Bcl-2. Then, up-regulated Bcl-2 was detected in OSCC tissues and cells compared with controls. Subsequently, Bcl-2-siRNA was found to be able to decrease cell viability while promote cell apoptosis in SCC9 cells, accompanied with the reduction of Bcl-2 and promotion of Bax. The Bcl-2/Bax ratio was reduced in Bcl-2-siRNA transfected group. In addition, miR-4262 mimic significantly suppressed the Bcl-2 expression, whereas the suppression was reversed by Bcl-2-plasmid. Furthermore, our results presented that miR-4262 mimic notably reduced cell viability and promoted cell apoptosis in SCC9 cell lines. Up-regulated miR-4262 could also downregulate Bcl-2 expression, upregulate the expression of Bax and decrease the Bcl-2/Bax ratio in SCC9 cells. However, Bcl-2-plasmid attenuated all these effects of miR-4262 mimic. Taken together, our findings indicated that miR-4262 exerted tumor-suppressive effects through targeting Bcl-2, resulting in promotion of cell apoptosis and inhibition of cell viability in OSCC cell lines. Therefore, miR-4262 might be a promising prognostic biomarker and novel therapeutic target during the therapy of OSCC.

Should Adolescents with NHL Be Treated as Old Children or Young Adults?

Hematology ◽  
2007 ◽  
Vol 2007 (1) ◽  
pp. 297-303 ◽  
Author(s):  
John T. Sandlund
Keyword(s):  
Young Adults ◽  
B Cell ◽  
Burkitt Lymphoma ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Lymphoblastic Lymphoma ◽  
Adolescents And Young Adults ◽  
Large B Cell Lymphoma ◽  
Age Related ◽  
Large B Cell

Abstract The SEER (Surveillance, Epidemiology, and End Results) data for the years 1975–1998 show that children with non-Hodgkin lymphoma (NHL) have a better treatment outcome than do adults. Many factors may contribute to this age-related difference. Some factors are related to the patient (e.g., drug distribution and clearance, performance status, compliance, sex) whereas others pertain to tumor histology and biology. The spectrum of NHL subtypes is well known to differ in children and adults. From ages 5 through 14 years, Burkitt lymphoma is the predominant histologic subtype, whereas diffuse large B-cell lymphoma is most common in the 15- to 29-year age range. Because different treatment strategies are often used in children and adults with NHL, the choice of therapy for adolescents and young adults (ages 15 through 29 years) is challenging and somewhat controversial. It is reasonable to consider pediatric strategies for some adolescents and very young adults with NHL, and pediatric strategies are currently used to treat adults with certain subtypes of NHL (Burkitt lymphoma, lymphoblastic lymphoma). However, the use of pediatric strategies in adults does not guarantee a comparable outcome, as illustrated by trials for adult lymphoblastic lymphoma. There is clearly a need for further biologic study of NHL in children, adolescents, and young adults. Age-related differences in tumor biology have been demonstrated in anaplastic large-cell lymphoma (ALCL) and diffuse large B-cell lymphoma (DLBCL). Additional biologic data will not only improve prognosis and treatment stratification but, more important, will lead to the identification of specific molecular targets for therapy.

ICT1 predicts a poor survival and correlated with cell proliferation in diffuse large B-cell lymphoma

Gene ◽  
2017 ◽  
Vol 627 ◽  
pp. 255-262 ◽  
Author(s):  
Wenjun Xie ◽  
Meijuan Wu ◽  
Tianhong Fu ◽  
Xiaohong Li ◽  
Zhaoming Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Poor Survival ◽  
Large B Cell Lymphoma ◽  
Large B Cell

scholarly journals PROLIFERATION AND APOPTOSIS OF B-CELL LYMPHOMA CELLS UNDER TARGETED REGULATION OF FOXO3 BY miR-155

2020 ◽  
Vol 12 (1) ◽  
pp. e2020073
Author(s):  
Xiaoqiang Zheng ◽  
Hongbing Rui ◽  
Ying Liu ◽  
Jinfeng Dong
Keyword(s):  
B Cell ◽  
B Lymphocytes ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Luciferase Reporter ◽  
Lymphoma Cells ◽  
Apoptosis Rate ◽  
Proliferation And Apoptosis ◽  
Low Expression

This study aimed to explore the proliferation and apoptosis of B-cell lymphoma cells under targeted regulation of FOXO3 by miR-155. We analyzed the differences between B-cell lymphoma cells and B lymphocytes in expressions of miR-155 and FOXO3, explored the effects of miR-155 on proliferation and apoptosis of B-cell lymphoma cells, and relevant mechanisms, and also analyzed the relationship between expressions of miR-155 and FOXO3 in 42 patients with diffuse large B-cell lymphoma (DLBCL) and clinical characteristics of them. B-cell lymphoma cells showed a higher expression of miR-155 and a low expression of FOXO3 than B lymphocytes (both P<0.05). B-cell lymphoma cells transfected with miR-155-inhibitor showed significantly decreased expression of miR-155, significantly weakened cell proliferation ability and increased cell apoptosis rate (all P<0.05), and they also showed up-regulated expression of FOXO3 (P<0.05). Dual luciferase reporter assay revealed that there were targeted binding sites between miR-155 and FOXO3. Compared with B-cell lymphoma cells transfected with miR-155-inhibitor alone, those with co-transfection showed lower expression of FOXO3, higher proliferation and lower cell apoptosis rate (all P<0.05). The expression of miR-155 in DLBCL tissues was higher than that in tumor-adjacent tissues (P<0.05), and the expressions of miR-155 and FOXO3 were closely related to the international prognostic index (IPI) and the 5-year prognosis and survival of the patients (P<0.05). miR-155 can promote the proliferation of B-cell lymphoma cells and suppress apoptosis of them by targeted inhibiting FOXO3, and both over-expression of miR-155 and low expression of FOXO3 are related to poor prognosis of DLBCL patients.

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