Cell proliferation and DNA content in non-hodgkin' s lymphoma: Flow cytometry in relation to lymphoma classification

Cancer ◽  
1986 ◽  
Vol 58 (6) ◽  
pp. 1295-1304 ◽  
Author(s):  
Birger Christensson ◽  
Bernhard Tribukait ◽  
Inga-Lill Under ◽  
Bengt Ullman ◽  
Peter Biberfeld
2011 ◽  
Vol 57 (1) ◽  
Author(s):  
Rikke Christensen ◽  
David M. Owens ◽  
Anette Thomsen ◽  
Søren Pedersen ◽  
Uffe Birk Jensen

Author(s):  
Terrence R. Tiersch ◽  
Robert W. Chandler ◽  
Klaus D. Kallman ◽  
Stephen S. Wachtel

2017 ◽  
Vol 44 (6) ◽  
pp. 2322-2336 ◽  
Author(s):  
Xitao Chen ◽  
Xiaodi Sun ◽  
Jingqian Guan ◽  
Junda Gai ◽  
Jilin Xing ◽  
...  

Background/Aims: The therapeutic efficacy of paclitaxel is hampered by chemotherapeutic resistance in non-small cell lung cancer (NSCLC). Rsf-1 enhanced paclitaxel resistance via nuclear factor-κB (NF-κB) in ovarian cancer cells and nasopharyngeal carcinoma. This study assessed the function of Rsf-1 in the modulation of the sensitivity of NSCLC to paclitaxel via the NF-κB pathway. Methods: The mRNA and protein levels of the related genes were quantified by RT-PCR and Western blotting. Rsf-1 silencing was achieved with CRISPR/Cas9 gene editing. Cell cycle, migration and proliferation were tested with flow cytometry, transwell test and CCK8 test. Cell apoptosis was analyzed with flow cytometry and quantification of C-capase3. The parameters of the tumors were measured in H460 cell xenograft mice. Results: Rsf-1 was highly expressed in H460 and H1299 cells. Rsf-1 knockout caused cell arrest at the G1 phase, increased cell apoptosis, and decreased migration and cell proliferation. Rsf-1 knockout increased the inhibition of cell proliferation, the reduction in cell migration and the augment in cell apoptosis in paclitaxel treated H460 and H1299 cells. Rsf-1 knockout further enhanced the paclitaxel-mediated decrease in the volume and weight of the tumors in H460 cell xenograft mice. Helenalin and Rsf-1 knockout decreased the protein levels of p-P65, BcL2, CFLAR, and XIAP; hSNF2H knockout decreased the protein level of NF-κB p-P65 without altering Rsf-1 and p65 protein levels, while Rsf-1 and hSNF2H double knockout decreased the level of NF-κB p-P65, in H1299 and H460 cells. Conclusion: These results demonstrate that Rsf-1 influences the sensitivity of NSCLC to paclitaxel via regulation of the NF-κB pathway and its downstream genes.


1998 ◽  
Vol 89 (6) ◽  
pp. 556-559 ◽  
Author(s):  
M Le Thierry d'Ennequin ◽  
O Panaud ◽  
S Brown ◽  
S Siljak-Yakovlev ◽  
A Sarr

2001 ◽  
Vol 197 (6) ◽  
pp. 411-418 ◽  
Author(s):  
Florence Le Pessot ◽  
Pierre Michel ◽  
Marianne Paresy ◽  
Françoise Lemoine ◽  
Marie-France Hellot ◽  
...  

2021 ◽  
Vol 7 (5) ◽  
pp. 3997-4004
Author(s):  
Zhibo Zou ◽  
Lin Peng

Objective: This study aimed to probe into the effect of LncRNA SNHG14 on ovarian cancer progression by regulating miR-206.Methods: Fifty-seven ovarian cancer (OC) patients who were treated in our hospital from December 2017 to December 2019 were collected as the research objects. During the operation, OC tissues and paracancerous tissues of patients were collected, and the effect of SNHG14 on OC tumor growth in nude mice was detected, and SNHG14 inhibitor was transfected into OC cells. The relative expression of SNHG14 in tissues and cells was detected by qRT-PCR, cell proliferation was testedvia CCK8, migration and invasion were detected through Transwell, apoptosis was assessedvia flow cytometry, and the targeted relationship between SNHG14 and miR-206 was detected by dual luciferase reporter gene.Results: SNHG14 is highly expressed in OC tissues, cells and nude mice. Down-regulating it can inhibit the biological ability of OC cells and inhibit the growth of nude mice tumors. It can directly target miR-206 to regulate CCND1 expression and promote OC progression.Conclusion: LncRNA SNHG14 can act as miR-206 sponge to regulate CCND1 expression downstream of miR-206 and promote OC progression.


2013 ◽  
Vol 790 ◽  
pp. 550-554
Author(s):  
Xiang Yu Zhou ◽  
Ya Jun Liu ◽  
Dan Li

Objective: p53, a tumor suppressor gene, is one of the hotspots in the world of the biomedical field. Mutation of p53 gene, which is found in approximately 50% of human cancers, is a key event in carcinogenesis. This project aims to investigate the new characteristics of two p53 mutants, p53-W248 and p53-H175, in MCF-7 cells, so as to provide the experimental basis for understanding the functional alternations of mutant p53. Methods: In this study, MCF-7 cells transfected with p53-H175 or p53-W248 plasmids were used as experimental group and the MCF-7 cells transfected wild type p53 plasmid were used as control group. Then the biological effects at the cellular level were investigated using 3-(4.5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay, flow cytometry analysis and cell scratch test. Results: MTT assay showed that p53-W248 might promote cell proliferation in MCF-7 cells. The results of flow cytometry indicated that no significant effect on cell cycle progression and cell apoptosis by p53-H175 or p53-W248 in cells. The cell scratch test showed that p53-H175 could increase the ability of cell migration. Conclusion: p53-H175 could lead to the promotion of tumor cell migration, while p53-W248 may promote tumor cell proliferation. p53-H175 and p53-W248 might have acquired some new characteristics of oncogenes.


Sign in / Sign up

Export Citation Format

Share Document