scholarly journals CD133, CD15/SSEA-1, CD34 or side populations do not resume tumor-initiating properties of long-term cultured cancer stem cells from human malignant glio-neuronal tumors

BMC Cancer ◽  
2010 ◽  
Vol 10 (1) ◽  
Author(s):  
Cristina Patru ◽  
Luciana Romao ◽  
Pascale Varlet ◽  
Laure Coulombel ◽  
Eric Raponi ◽  
...  
2019 ◽  
Vol 13 (5) ◽  
pp. 1311-1331 ◽  
Author(s):  
Alicia Bort ◽  
Belén G. Sánchez ◽  
Pedro A. Mateos‐Gómez ◽  
Diana Vara‐Ciruelos ◽  
Nieves Rodríguez‐Henche ◽  
...  

2009 ◽  
Vol 219 (2) ◽  
pp. 301-313 ◽  
Author(s):  
Riccardo Di Fiore ◽  
Andrea Santulli ◽  
Rosa Drago Ferrante ◽  
Michela Giuliano ◽  
Anna De Blasio ◽  
...  

2020 ◽  
Vol 21 (1) ◽  
pp. 1-1
Author(s):  
Yuji Tanimura ◽  
Toshiro Fukui ◽  
Shunsuke Horitani ◽  
Yasushi Matsumoto ◽  
Sachi Miyamoto ◽  
...  

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Sandra Valle ◽  
Sonia Alcalá ◽  
Laura Martin-Hijano ◽  
Pablo Cabezas-Sáinz ◽  
Diego Navarro ◽  
...  

Abstract Pancreatic ductal adenocarcinoma (PDAC), the fourth leading cause of cancer death, has a 5-year survival rate of approximately 7–9%. The ineffectiveness of anti-PDAC therapies is believed to be due to the existence of a subpopulation of tumor cells known as cancer stem cells (CSCs), which are functionally plastic, and have exclusive tumorigenic, chemoresistant and metastatic capacities. Herein, we describe a 2D in vitro system for long-term enrichment of pancreatic CSCs that is amenable to biological and CSC-specific studies. By changing the carbon source from glucose to galactose in vitro, we force PDAC cells to utilize OXPHOS, resulting in enrichment of CSCs defined by increased CSC biomarker and pluripotency gene expression, greater tumorigenic potential, induced but reversible quiescence, increased OXPHOS activity, enhanced invasiveness, and upregulated immune evasion properties. This CSC enrichment method can facilitate the discovery of new CSC-specific hallmarks for future development into targets for PDAC-based therapies.


2013 ◽  
Vol 2013 ◽  
pp. 1-5
Author(s):  
Peng Tang ◽  
Aijun Fan ◽  
Jianquan Li ◽  
Jun Jiang ◽  
Kaifa Wang

To quantitatively study the effect of delay on selection dynamics in long-term sphere culture of cancer stem cells (CSCs), a selection dynamic model with time delay is proposed. Theoretical results show that the ubiquitous time delay in cell proliferation may be one of the important factors to induce fluctuation, and numerical simulations indicate that the proposed selection dynamical model with time delay can provide a better fitting effect for the experiment of a long-term sphere culture of CSCs. Thus, it is valuable to consider the delay effect in the future study on the dynamics of nongenetic heterogeneity of clonal cell populations.


Theranostics ◽  
2017 ◽  
Vol 7 (19) ◽  
pp. 4805-4824 ◽  
Author(s):  
Xiaoti Lin ◽  
Weiyu Chen ◽  
Fengqin Wei ◽  
Binhua P. Zhou ◽  
Mien-Chie Hung ◽  
...  

2021 ◽  
Author(s):  
Masahiro Shimizu ◽  
Hiroshi Shibuya ◽  
Nobuyuki Tanaka

Abstract Cancer stem cells (CSCs) have tumour initiation, self-renewal, and long-term tumour repopulation properties, and it is postulated that differentiated somatic cells can be reprogrammed to CSCs by oncogenic signals. We previously showed that oncogenic HRASV12 conferred tumour initiation capacity in tumour suppressor p53-deficient (p53−/−) primary mouse embryonic fibroblasts (MEFs) through transcription factor NF-κB-mediated enhancement of glucose uptake; however, the underlying mechanisms of RAS oncogene-induced CSC reprogramming have not been elucidated. Here, we found that the expression of the reprogramming factor SOX2 was induced by HRASV12 in p53−/− MEFs. Moreover, gene knockout studies revealed that SOX2 is an essential factor for the generation of CSCs by HRASV12 in mouse and human fibroblasts. We demonstrated that HRASV12-induced cyclin-dependent kinase 1 (CDK1) activity and subsequent enhancement of protein O-GlcNAcylation were required for SOX2 induction and CSC generation in these fibroblasts and cancer cell lines containing RAS mutations. Moreover, the CDK inhibitor dinaciclib and O-GlcNAcylation inhibitor OSMI1 reduced the number of CSCs derived from these cells. Taken together, our results reveal a signalling pathway and mechanism for CSC generation by oncogenic RAS and suggest the possibility that this signalling pathway is a therapeutic target for CSCs.


2005 ◽  
Vol 65 (8) ◽  
pp. 3126-3135 ◽  
Author(s):  
Jorge S. Burns ◽  
Basem M. Abdallah ◽  
Per Guldberg ◽  
Jørgen Rygaard ◽  
Henrik D. Schrøder ◽  
...  

2018 ◽  
Vol 2 (1) ◽  
Author(s):  
Abdulmajeed Almutary

Solid tumours are an immense cancer burden and a main therapeutic challenge. The theory of cancer stem cells provides an attractive cellular mechanism to account for the therapeutic resistance exhibited by many of these tumours. There is strong evidence that various solid tumours are hierarchically managed and sustained by notable subpopulations of cancer stem cells. Recent evidence of cancer stem cells emerged from a mouse model epithelial tumorigenesis, also some models of heterogeneity may apply. Haematopoietic stem cells (HSCs) have the capability to renew themselves and produce lineages of the blood; yet the signals that control HSc self-renewal remain indistinct. WnT signalling pathway has crucial role in the expression of activated p-catenin which expands the HSCs in a long-term cultures. In addition, Wnt signalling can interrupt the lymphocyte progenitor cells proliferation and affect the cells development. Other similar signalling pathways such as Notch and Hedgehog (Hh) are found in normal stem cells. Therapeutic targeting of cancer stem cells and tumour population could shed light on how to supress tumour growth. In this review, we suggest that by developing a new anti-cancer stem cell therapeutic agent that targets embryonic signalling pathways of cancer stem cells can improve the treatment of the disease


PLoS ONE ◽  
2011 ◽  
Vol 6 (11) ◽  
pp. e25518 ◽  
Author(s):  
Tang Peng ◽  
Ma Qinghua ◽  
Tang Zhenning ◽  
Wang Kaifa ◽  
Jiang Jun

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