scholarly journals miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma

2019 ◽  
Vol Volume 11 ◽  
pp. 2739-2746 ◽  
Author(s):  
Yiqun Huang ◽  
Yong Zou ◽  
Luhui Lin ◽  
Xudong Ma ◽  
Ruiji Zheng
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Large B Cell Lymphoma ◽  
Proliferation And Apoptosis ◽  
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

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.

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 The Stimulatory Role of CD300a in Diffuse Large B-Cell Lymphoma

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 2975-2975
Author(s):  
Lei Jiang ◽  
Jeff Xiwu Zhou ◽  
Herbert Morse ◽  
Yulian Xu
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Inhibitory Effect ◽  
Type I ◽  
Expression Levels ◽  
Large B Cell Lymphoma ◽  
Large B Cell

Abstract CD300a is a type I transmembrane receptor protein which has shown inhibitory effect on B-cell receptor mediated signals. In an analysis of publicly available data on diffuse large B-cell lymphoma (DLBCL), however, we found that the expression levels of CD300A mRNA were inversely correlated with the overall survival of DLBCL patients. When analyzing the transcript levels of CD300a in human tissues, we found that CD300a mRNA levels were significantly greater in DLBCL tissues than benign lymphoid tissues (P<0.05). To decipher the role of CD300a in DLBCL, we used shRNA system to knock-down the expression levels of CD300a in DLBCL cell lines, and found that decreased levels of CD300a significantly inhibited cell proliferation of OCI-Ly1 cells, but not of VAL, OCI-Ly10 or SUDHL-8 cells. Mechanistically, reduced expression of CD300a resulted in a marked attenuation of Akt phosphorylation in OCI-Ly1 cells. Pharmacologic inhibition of PI3K by LY294002 displayed a similar inhibitory effect on cell proliferation, indicating the possible involvement of PI3K/Akt signaling pathway in CD300a’s effect. Furthermore, using a xenograft animal model, we found that decreasing expression levels of CD300a in OCI-Ly1 cells significantly inhibited tumor formation of these cells in vivo. Collectively, our results suggested a stimulatory role of CD300a in DLBCL which could serve as a potential biomarker and therapeutic target for this malignance. Disclosures No relevant conflicts of interest to declare.

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