Identification and expansion of human osteosarcoma-cancer-stem cells by long-term 3-aminobenzamide treatment

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

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 ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Neuronal Tumors

scholarly journals Targeting AMP ‐activated kinase impacts hepatocellular cancer stem cells induced by long‐term treatment with sorafenib

2019 ◽  
Vol 13 (5) ◽  
pp. 1311-1331 ◽  
Author(s):  
Alicia Bort ◽  
Belén G. Sánchez ◽  
Pedro A. Mateos‐Gómez ◽  
Diana Vara‐Ciruelos ◽  
Nieves Rodríguez‐Henche ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Hepatocellular Cancer ◽  
Term Treatment ◽  
Long Term Treatment

scholarly journals Long‑term model of colitis‑associated colorectal cancer suggests tumor spread mechanism and nature of cancer stem cells

2020 ◽  
Vol 21 (1) ◽  
pp. 1-1
Author(s):  
Yuji Tanimura ◽  
Toshiro Fukui ◽  
Shunsuke Horitani ◽  
Yasushi Matsumoto ◽  
Sachi Miyamoto ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Tumor Spread ◽  
Term Model

scholarly journals Exploiting oxidative phosphorylation to promote the stem and immunoevasive properties of pancreatic cancer stem cells

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Sandra Valle ◽  
Sonia Alcalá ◽  
Laura Martin-Hijano ◽  
Pablo Cabezas-Sáinz ◽  
Diego Navarro ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Ductal Adenocarcinoma ◽  
In Vitro System ◽  
Tumorigenic Potential ◽  
Term Enrichment ◽  
Pluripotency Gene ◽  
Pancreatic Cancer Stem Cells

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.

scholarly journals Effect of Delay on Selection Dynamics in Long-Term Sphere Culture of Cancer Stem Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-5
Author(s):  
Peng Tang ◽  
Aijun Fan ◽  
Jianquan Li ◽  
Jun Jiang ◽  
Kaifa Wang
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Time Delay ◽  
Cancer Stem Cells ◽  
Cell Populations ◽  
Delay Effect ◽  
Selection Dynamics ◽  
Sphere Culture ◽  
Theoretical Results

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.

scholarly journals Mutant p53 gain of function can be at the root of dedifferentiation of human osteosarcoma MG63 cells into 3AB-OS cancer stem cells

Bone ◽  
2014 ◽  
Vol 60 ◽  
pp. 198-212 ◽  
Author(s):  
Riccardo Di Fiore ◽  
Michela Marcatti ◽  
Rosa Drago-Ferrante ◽  
Antonella D'Anneo ◽  
Michela Giuliano ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Mutant P53 ◽  
Gain Of Function ◽  
Human Osteosarcoma ◽  
Mg63 Cells

scholarly journals MicroRNA-29b-1 impairs in vitro cell proliferation, self-renewal and chemoresistance of human osteosarcoma 3AB-OS cancer stem cells

2014 ◽  
Vol 45 (5) ◽  
pp. 2013-2023 ◽  
Author(s):  
RICCARDO DI FIORE ◽  
ROSA DRAGO-FERRANTE ◽  
FRANCESCA PENTIMALLI ◽  
DOMENICO DI MARZO ◽  
IRIS MARIA FORTE ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Cancer Stem Cells ◽  
Self Renewal ◽  
Human Osteosarcoma

scholarly journals Nanoparticle Delivery of miR-34a Eradicates Long-term-cultured Breast Cancer Stem Cells via Targeting C22ORF28 Directly

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

scholarly journals Oncogenic RAS Generates Cancer Stem Cells in p53-Deficient Fibroblasts Through SOX2 Induced By CDK1-Mediated Protein O-GlcNAcylation

2021 ◽  
Author(s):  
Masahiro Shimizu ◽  
Hiroshi Shibuya ◽  
Nobuyuki Tanaka
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Gene Knockout ◽  
Human Fibroblasts ◽  
Signalling Pathway ◽  
Oncogenic Ras ◽  
Primary Mouse ◽  
Underlying Mechanisms ◽  
Tumour Initiation

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.

Tumorigenic Heterogeneity in Cancer Stem Cells Evolved from Long-term Cultures of Telomerase-Immortalized Human Mesenchymal Stem Cells

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