microRNA‑196a‑3p inhibits cell proliferation and promotes cell apoptosis by targeting ADP ribosylation factor 4 in diffuse large B‑cell lymphoma

2020 ◽  
Vol 45 (2) ◽  
pp. 764-775
Author(s):  
Jianhong Fu ◽  
Xiaoli Lou ◽  
Shan Wan ◽  
Xin Zhao ◽  
Zhi Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Adp Ribosylation ◽  
Large B Cell Lymphoma ◽  
Adp Ribosylation Factor ◽  
Large B Cell

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

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

Effect of siRNA interference of ubiquitin-specific protease 9X on apoptosis and growth of diffuse large B cell lymphoma cell line

2020 ◽  
Vol 10 (3) ◽  
pp. 446-453
Author(s):  
Wei Peng ◽  
Meizuo Zhong ◽  
Youhong Tang
Keyword(s):  
B Cells ◽  
Protein Expression ◽  
B Cell ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Large B Cell Lymphoma ◽  
Specific Protease ◽  
Sirna Interference ◽  
Large B Cell

Ubiquitin-specific protease 9X (USP9X) is crucial in the diagnosis and treatment of many tumor types, but its role in Diffuse Large B Cell Lymphoma (DLBCL) has not been determined. The current study aimed to examine the effects of RNA interference on USP9X expression, and subsequently on the bioactivity of DLBCL Farage and Pfeiffer cells. There were two groups in the study: USP9X-siRNA and NC. USP9X siRNA was transiently transferred into DLBCL cells by Cationic liposome. The total RNA was extracted using Fe2O3 and was retrieved into the DNA using the MagBeads Total RNA Extraction Kit. The protein expression of USP9X in Farage, Pfeiffer, and normal human B cell line at the cellular level was observed by Western blot. The Farage and Pfeiffer cells were infected with USP9X-siRNA. Cell apoptosis and cell growth viability were analyzed by flow cytometry and CCK8, Mcl-1 protein, a potential target of USP9X, and apoptosis factor proteins (such as Bak, Cytochrome C, Caspase 3, Caspase 8, PARP) were detected by Western blot after siRNA interference. The results showed that the protein expression of USP9X in malignant B cells was four times higher than that of the normal B cells. Inhibition of USP9X reduced the Mcl-1 activity, and increased the caspase-3, Bak and Cytochrome C activity. In the malignant B cells, Mcl-1 and Bak were binding in vivo; Bak was a new partner of Mcl-1. Inhibition of USP9X reduced cell proliferation and increased apoptosis. The expression of USP9X is upregulated in Diffuse large B cell lymphoma cells, Farage, and Pfeiffer. Inhibition expression of USP9X may induce cell apoptosis, inhibit cell growth, and downregulate Mcl-1 protein expression in Diffuse large B cell lymphoma cells, Farage, and Pfeiffer. USP9X has the ability in regulating cell apoptosis.

Loss of IRF8 Inhibits the Growth of Diffuse Large B-Cell Lymphoma

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 3004-3004
Author(s):  
Yulian Xu ◽  
Lei Jiang ◽  
Rachel R. Fang ◽  
Jeff Xiwu Zhou ◽  
Herbert Morse
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Cell Lymphoma ◽  
Critical Role ◽  
B Cell Lymphoma ◽  
Expression Levels ◽  
Large B Cell Lymphoma ◽  
Large B Cell

Abstract IRF8 is a transcription factor with a critical role in B lymphocyte development and biological functions. Although it has been reported that IRF8 is highly expressed in human diffuse large B-cell lymphoma (DLBCL) and the translocation of IRF8-IgH loci occurs in DLBCL, little information is available regarding the function and mechanisms for the role of IRF8 in DLBCL. In this study, by using several human DLBCL cell lines with shRNA-mediated decrease in IRF8 expression levels, we found that the loss of IRF8 significantly reduced the proliferation of lymphoma cells (Figure 1). Mechanistically, decreasing the levels of IRF8 led to a decrease in p38 and ERK phosphorylation (Figure 2), molecular events critical for B cell proliferation. Furthermore, using a xenograft lymphoma mice model, we found that the loss of IRF8 significantly inhibited the growth of lymphomas in vivo (n=5 for each group) (Figure 3). Analysis of public available data also suggested that the expression levels of IRF8 mRNA in human DLBCL tissues were inversely correlated patientsÕ overall survival time. Taken together, this study showed that IRF8 may play an oncogenic role in human DLBCL by promoting cell proliferation. Figure 1. Loss of IRF8 decreased the proliferation of DLBCL cells in vitro. Figure 1. Loss of IRF8 decreased the proliferation of DLBCL cells in vitro. Figure 2. Loss of IRF8 decreased the phosphorylation of p38 and ERK in DLBCL cells. Figure 2. Loss of IRF8 decreased the phosphorylation of p38 and ERK in DLBCL cells. Figure 3. Loss of IRF8 decreased the growth of DLBCL in vivo. Figure 3. Loss of IRF8 decreased the growth of DLBCL in vivo. Disclosures No relevant conflicts of interest to declare.

scholarly journals Effects of 17-DMAG on diffuse large B-cell lymphoma cell apoptosis

2017 ◽  
Vol 14 (4) ◽  
pp. 3727-3731 ◽  
Author(s):  
Jia-Jia Li ◽  
Jing-Jing Zhang ◽  
Xiu Wang ◽  
Zi-Min Sun
Keyword(s):  
B Cell ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Lymphoma Cell ◽  
Large B Cell Lymphoma ◽  
Large B Cell
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