MicroRNAs and cancer stem cells: Therapeutic approaches and future perspectives

2013 ◽  
Vol 338 (1) ◽  
pp. 174-183 ◽  
Author(s):  
J.A. Leal ◽  
M.E. Lleonart
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Future Perspectives ◽  
Therapeutic Approaches

scholarly journals LSD1/KDM1A, a Gate-Keeper of Cancer Stemness and a Promising Therapeutic Target

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1821 ◽  
Author(s):  
Panagiotis Karakaidos ◽  
John Verigos ◽  
Angeliki Magklara
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cellular Reprogramming ◽  
Future Perspectives ◽  
Cancer Stemness ◽  
Neuronal Stem Cells ◽  
Lysine Specific Demethylase ◽  
Promising Therapeutic Target ◽  
Exciting Area ◽  
Established Role

A new exciting area in cancer research is the study of cancer stem cells (CSCs) and the translational implications for putative epigenetic therapies targeted against them. Accumulating evidence of the effects of epigenetic modulating agents has revealed their dramatic consequences on cellular reprogramming and, particularly, reversing cancer stemness characteristics, such as self-renewal and chemoresistance. Lysine specific demethylase 1 (LSD1/KDM1A) plays a well-established role in the normal hematopoietic and neuronal stem cells. Overexpression of LSD1 has been documented in a variety of cancers, where the enzyme is, usually, associated with the more aggressive types of the disease. Interestingly, recent studies have implicated LSD1 in the regulation of the pool of CSCs in different leukemias and solid tumors. However, the precise mechanisms that LSD1 uses to mediate its effects on cancer stemness are largely unknown. Herein, we review the literature on LSD1’s role in normal and cancer stem cells, highlighting the analogies of its mode of action in the two biological settings. Given its potential as a pharmacological target, we, also, discuss current advances in the design of novel therapeutic regimes in cancer that incorporate LSD1 inhibitors, as well as their future perspectives.

scholarly journals Therapeutic Approaches to Target Cancer Stem Cells

Cancers ◽  
2011 ◽  
Vol 3 (3) ◽  
pp. 3331-3352 ◽  
Author(s):  
Arlhee Diaz ◽  
Kalet Leon
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Therapeutic Approaches ◽  
Target Cancer

scholarly journals Co-Expression of CD34, CD90, OV-6 and Cell-Surface Vimentin Defines Cancer Stem Cells of Hepatoblastoma, Which Are Affected by Hsp90 Inhibitor 17-AAG

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2598
Author(s):  
Mieun Lee-Theilen ◽  
Julia R. Hadhoud ◽  
Giulietta Volante ◽  
Delaine D. Fadini ◽  
Julia Eichhorn ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Surface ◽  
Hsp90 Inhibitor ◽  
Chemotherapeutic Drug ◽  
Therapeutic Approaches ◽  
Pediatric Solid Tumors ◽  
Tumor Research ◽  
And Migration ◽  
Emt Markers

Cancer stem cells (CSCs) are nowadays one of the major focuses in tumor research since this subpopulation was revealed to be a great obstacle for successful treatment. The identification of CSCs in pediatric solid tumors harbors major challenges because of the immature character of these tumors. Here, we present CD34, CD90, OV-6 and cell-surface vimentin (csVimentin) as reliable markers to identify CSCs in hepatoblastoma cell lines. We were able to identify CSC characteristics for the subset of CD34+CD90+OV-6+csVimentin+-co-expressing cells, such as pluripotency, self-renewal, increased expression of EMT markers and migration. Treatment with Cisplatin as the standard chemotherapeutic drug in hepatoblastoma therapy further revealed the chemo-resistance of this subset, which is a main characteristic of CSCs. When we treated the cells with the Hsp90 inhibitor 17-AAG, we observed a significant reduction in the CSC subset. With our study, we identified CSCs of hepatoblastoma using CD34, CD90, OV-6 and csVimentin. This set of markers could be helpful to estimate the success of novel therapeutic approaches, as resistant CSCs are responsible for tumor relapses.

scholarly journals Therapeutic approaches targeting cancer stem cells

2018 ◽  
Vol 14 (7) ◽  
pp. 1469 ◽  
Author(s):  
Chuanwu Zhu ◽  
Yunzhi Pan ◽  
Sai Ma ◽  
Kaiyue Cao ◽  
Sufang Zhou ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Therapeutic Approaches

scholarly journals TLR-4 Signaling vs. Immune Checkpoints, miRNAs Molecules, Cancer Stem Cells, and Wingless-Signaling Interplay in Glioblastoma Multiforme—Future Perspectives

2020 ◽  
Vol 21 (9) ◽  
pp. 3114 ◽  
Author(s):  
Jakub Litak ◽  
Cezary Grochowski ◽  
Joanna Litak ◽  
Ida Osuchowska ◽  
Krzysztof Gosik ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Immune Checkpoints ◽  
Toll Like Receptor ◽  
Future Perspectives ◽  
Programmed Death Ligand 1 ◽  
Incurable Disease ◽  
Programmed Death ◽  
Strong Relation ◽  
The Central Nervous System

Toll-like-receptor (TLR) family members were detected in the central nervous system (CNS). TLR occurrence was noticed and widely described in glioblastomamultiforme (GBM) cells. After ligand attachment, TLR-4 reorients domains and dimerizes, activates an intracellular cascade, and promotes further cytoplasmatic signaling. There is evidence pointing at a strong relation between TLR-4 signaling and micro ribonucleic acid (miRNA) expression. The TLR-4/miRNA interplay changes typical signaling and encourages them to be a target for modern immunotherapy. TLR-4 agonists initiate signaling and promote programmed death ligand-1 (PD-1L) expression. Most of those molecules are intensively expressed in the GBM microenvironment, resulting in the autocrine induction of regional immunosuppression. Another potential target for immunotreatment is connected with limited TLR-4 signaling that promotes Wnt/DKK-3/claudine-5 signaling, resulting in a limitation of GBM invasiveness. Interestingly, TLR-4 expression results in bordering proliferative trends in cancer stem cells (CSC) and GBM. All of these potential targets could bring new hope for patients suffering from this incurable disease. Clinical trials concerning TLR-4 signaling inhibition/promotion in many cancers are recruiting patients. There is still a lot to do in the field of GBM immunotherapy.

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