scholarly journals The pro-cell death Bcl-2 family member, BNIP3, is localized to the nucleus of human glial cells: Implications for glioblastoma multiforme tumor cell survival under hypoxia

2006 ◽  
Vol 118 (7) ◽  
pp. 1660-1669 ◽  
Author(s):  
Teralee R. Burton ◽  
Elizabeth S. Henson ◽  
Priti Baijal ◽  
David D. Eisenstat ◽  
Spencer B. Gibson
Keyword(s):  
Cell Death ◽  
Glioblastoma Multiforme ◽  
Tumor Cell ◽  
Cell Survival ◽  
Family Member ◽  
Glial Cells ◽  
Tumor Cell Survival

Cell-Cell Communication Between Multiple Myeloma (MM) Cells and Cord Blood Derived NK Cells (CB-NK) Regulates Both Tumor Cell Death and Tumor Cell Survival

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 1787-1787
Author(s):  
Beatriz Martin-Antonio ◽  
Erica Serrano ◽  
Guillermo Suñe ◽  
Lorena Perez ◽  
Marcos Calderón ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Cell ◽  
Cell Survival ◽  
Nk Cells ◽  
Cell Communication ◽  
K562 Cells ◽  
Tumor Cell Survival ◽  
Nk Cytotoxicity ◽  
Lipid Structures ◽  
Cell Cell

Abstract In previous work we have demonstrated that CB-NK exert a cytotoxicity towards MM cells which involves lipid-protein vesicle transfer, which it is secondarily transferred from recipient MM cells to neighboring MM cells. This transmissible cytotoxicity causes a 5-7% of neighboring MM cell death (CDD 2015;22(1):96-107). However, this transmission between MM cells could have a diluent effect of the CB-NK cytotoxicity which could be also a tumor cell survival mechanism. To further analyze this mechanism, we determined the proteins transferred between cells and the role of lipids in this transfer. We performed TRANS-SILAC proteomics using two different approaches: 1) Labeling CB-NK cells with heavy amino-acids (hAA) to identify both CB-NK proteins transferred to MM (1ºMM) and secondary CB-NK proteins transferred from 1ºMM to neighboring MM cells (2ºMM). 2) Labeling MM cells, before CB-NK contact, with hAA to identify transferred proteins from 1ºMM to 2ºMM cells, and from 1ºMM to CB-NK. We found that 1ºMM cells acquired 9.5% of CB-NK proteins, and that these proteins were transferred to 2ºMM cells. As a consequence, 1ºMM cells diluted the CB-NK proteins from 9.5% to 3.8%; which represented 7.2% of proteins in 2ºMM cells. In the second approach, we observed that, MM cells transferred to neighboring MM cells only 1.9% of MM proteins in resting conditions. However, in the presence of CB-NK, this transfer was increased up to 7.7%. Furthermore, CB-NK cells acquired 7.3% of 1ºMM proteins. These findings demonstrate a secondary CB-NK protein transfer between MM cells, which represents a CB-NK protein dilution content from 1ºMM to 2ºMM, and an increased transfer of 1ºMM proteins to 2ºMM (Fig.1A). Proteomic analysis showed that transferred proteins were involved in FAS signaling, apoptosis, inflammation, chromatin organization, glycolysis, spliceosome, and rRNA metabolic process. Among these proteins we focused on histones and the 14-3-3 family which are associated to both cell death and cell survival. Confocal microscopy confirmed transfer of histones and 14-3-3 proteins. Protein transfer occurred within neutral lipid vesicles-structures. We also observed that MM cells were inter-connected with a much higher number of neutral lipid structures (nanotubes and bigger structures similar to bags) than in K562 cells (Fig. 1B). Thus, we next analyzed the role of these neutral lipids in MM cell-cell communication. The cholesterol synthesis and lipid transport inhibitor U18666A significantly decreased the number of these lipid connective structures between MM cells, and it was toxic for MM cells. Furthermore, breaking the lipid connection between MM cells with U18666A increased CB-NK cytotoxicity (p<0.05). These effects were not observed in K562 cells. This could be explained by a blockage of the diluent effect mediated by MM cells of the proteins and lipids from CB-NK cells. Last, we analyzed apoptotic levels of 1ºMM cells after co-culture with 2ºMM cells, and the apoptotic levels of the remaining 2ºMM cells. Both populations became early apoptotic, however, after 3-5 days they recovered from early apoptosis, decreasing from 36% of early apoptotic cells to 3%, which was their apoptotic basal levels, and most importantly, without causing cell death, as no difference in the cell number in comparison to control MM cells was observed. Therefore, our data demonstrate that this diluent transmission effect between MM cells might be a new cell mechanism that contributes to tumor cell survival. Importantly, because lipid structures mediate this diluent transmission effect, this tumor cell survival mechanism might be eliminated by using lipid metabolism inhibitors. In conclusion, cell-cell communication increases when MM cells are stressed because of CB-NK presence. Although this causes a transmissible cytotoxicity in a small % of MM cells, a diluent effect also occurs between cells helping MM cells to recover and promoting MM cell survival. Lipid structures play an important role in this cell-cell communication, which may represent a new therapeutic target for MM treatment. Disclosures No relevant conflicts of interest to declare.

scholarly journals Pim1 kinase is upregulated in glioblastoma multiforme and mediates tumor cell survival

2014 ◽  
Vol 17 (2) ◽  
pp. 223-242 ◽  
Author(s):  
Susann Herzog ◽  
Matthias Alexander Fink ◽  
Kerstin Weitmann ◽  
Claudius Friedel ◽  
Stefan Hadlich ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
Tumor Cell ◽  
Cell Survival ◽  
Pim1 Kinase ◽  
Tumor Cell Survival

scholarly journals A gene expression signature associated with ‘‘K-Ras addiction’’ reveals regulators of EMT and tumor cell survival

Cancer Cell ◽  
2021 ◽  
Vol 39 (3) ◽  
pp. 441-442
Author(s):  
Anurag Singh ◽  
Patricia Greninger ◽  
Daniel Rhodes ◽  
Louise Koopman ◽  
Sheila Violette ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Cell ◽  
Cell Survival ◽  
Gene Expression Signature ◽  
Expression Signature ◽  
Tumor Cell Survival

Brain-Derived Neurotrophic Factor and Neurotrophin-4/5 Are Expressed in Breast Cancer and Can Be Targeted to Inhibit Tumor Cell Survival

2011 ◽  
Vol 17 (7) ◽  
pp. 1741-1752 ◽  
Author(s):  
Elsa Vanhecke ◽  
Eric Adriaenssens ◽  
Stéphanie Verbeke ◽  
Samuel Meignan ◽  
Emmanuelle Germain ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cell ◽  
Cell Survival ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Tumor Cell Survival

scholarly journals TMEM74 promotes tumor cell survival by inducing autophagy via interactions with ATG16L1 and ATG9A

2017 ◽  
Vol 8 (8) ◽  
pp. e3031-e3031 ◽  
Author(s):  
Yizhe Sun ◽  
Yingyu Chen ◽  
Jingyu Zhang ◽  
Lulu Cao ◽  
Minwei He ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Survival ◽  
Tumor Cell Survival

scholarly journals Sonic Hedgehog Promotes Tumor Cell Survival by Inhibiting CDON Pro-Apoptotic Activity

PLoS Biology ◽  
2013 ◽  
Vol 11 (8) ◽  
pp. e1001623 ◽  
Author(s):  
Céline Delloye-Bourgeois ◽  
Benjamin Gibert ◽  
Nicolas Rama ◽  
Jean-Guy Delcros ◽  
Nicolas Gadot ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Survival ◽  
Sonic Hedgehog ◽  
Tumor Cell Survival ◽  
Apoptotic Activity
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