scholarly journals The high expression of miR-31 in lung adenocarcinoma inhibits the malignancy of lung adenocarcinoma tumor stem cells

2021 ◽  
Vol 28 ◽  
pp. 101122
Author(s):  
Ran Xu ◽  
Tianhua Liu ◽  
Ling Zuo ◽  
Dongqing Guo ◽  
Guancheng Ye ◽  
...  
Keyword(s):  
Stem Cells ◽  
Lung Adenocarcinoma ◽  
High Expression ◽  
Tumor Stem Cells

Therapeutic Role of Bmi-1 Inhibitors in Eliminating Prostate Tumor Stem Cells

2013 ◽  
Author(s):  
Isaac Y. Kim ◽  
Joseph Bertino ◽  
Hatem E. Sabaawy
Keyword(s):  
Stem Cells ◽  
Prostate Tumor ◽  
Tumor Stem Cells ◽  
Therapeutic Role

scholarly journals The Importance of Tumor Stem Cells in Glioblastoma Resistance to Therapy

2021 ◽  
Vol 22 (8) ◽  
pp. 3863
Author(s):  
Vincenzo Mattei ◽  
Francesca Santilli ◽  
Stefano Martellucci ◽  
Simona Delle Monache ◽  
Jessica Fabrizi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Radical Surgery ◽  
Cellular Heterogeneity ◽  
Molecular Characteristics ◽  
Tumor Stem Cells ◽  
Current Standard ◽  
New Approach ◽  
Experimental Therapies ◽  
Technical Advances ◽  
New Anticancer Drugs

Glioblastoma (GBM) is known to be the most common and lethal primary malignant brain tumor. Therapies against this neoplasia have a high percentage of failure, associated with the survival of self-renewing glioblastoma stem cells (GSCs), which repopulate treated tumors. In addition, despite new radical surgery protocols and the introduction of new anticancer drugs, protocols for treatment, and technical advances in radiotherapy, no significant improvement in the survival rate for GBMs has been realized. Thus, novel antitarget therapies could be used in conjunction with standard radiochemotherapy approaches. Targeted therapy, indeed, may address specific targets that play an essential role in the proliferation, survival, and invasiveness of GBM cells, including numerous molecules involved in signal transduction pathways. Significant cellular heterogeneity and the hierarchy with GSCs showing a therapy-resistant phenotype could explain tumor recurrence and local invasiveness and, therefore, may be a target for new therapies. Therefore, the forced differentiation of GSCs may be a promising new approach in GBM treatment. This article provides an updated review of the current standard and experimental therapies for GBM, as well as an overview of the molecular characteristics of GSCs, the mechanisms that activate resistance to current treatments, and a new antitumor strategy for treating GSCs for use as therapy.

scholarly journals Bioinformatics study on genes related to a high-risk postoperative recurrence of lung adenocarcinoma

2021 ◽  
Vol 104 (3) ◽  
pp. 003685042110180
Author(s):  
Xiao Lin ◽  
Meng Zhou ◽  
Zehong Xu ◽  
Yusheng Chen ◽  
Fan Lin
Keyword(s):  
Cell Cycle ◽  
Gene Ontology ◽  
High Risk ◽  
Lung Adenocarcinoma ◽  
Candidate Genes ◽  
Postoperative Recurrence ◽  
High Expression ◽  
Ppi Network ◽  
Hub Genes ◽  
Expression Levels

In this study, we aimed to screen out genes associated with a high risk of postoperative recurrence of lung adenocarcinoma and investigate the possible mechanisms of the involvement of these genes in the recurrence of lung adenocarcinoma. We identify Hub genes and verify the expression levels and prognostic roles of these genes. Datasets of GSE40791, GSE31210, and GSE30219 were obtained from the Gene Expression Omnibus database. Enrichment analysis of gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were performed for the screened candidate genes using the DAVID database. Then, we performed protein–protein interaction (PPI) network analysis through the database STRING. Hub genes were screened out using Cytoscape software, and their expression levels were determined by the GEPIA database. Finally, we assessed the relationships of Hub genes expression levels and the time of survival. Forty-five candidate genes related to a high-risk of lung adenocarcinoma recurrence were screened out. Gene ontology analysis showed that these genes were enriched in the mitotic spindle assembly checkpoint, mitotic sister chromosome segregation, G2/M-phase transition of the mitotic cell cycle, and ATP binding, etc. KEGG analysis showed that these genes were involved predominantly in the cell cycle, p53 signaling pathway, and oocyte meiosis. We screened out the top ten Hub genes related to high expression of lung adenocarcinoma from the PPI network. The high expression levels of eight genes (TOP2A, HMMR, MELK, MAD2L1, BUB1B, BUB1, RRM2, and CCNA2) were related to short recurrence-free survival and they can be used as biomarkers for high risk of lung adenocarcinoma recurrence. This study screened out eight genes associated with a high risk of lung adenocarcinoma recurrence, which might provide novel insights into researching the recurrence mechanisms of lung adenocarcinoma as well as into the selection of targets in the treatment of the disease.

scholarly journals Antigenic and Genotypic Similarity between Primary Glioblastomas and Their Derived Neurospheres

2011 ◽  
Vol 2011 ◽  
pp. 1-16 ◽  
Author(s):  
Valentina Caldera ◽  
Marta Mellai ◽  
Laura Annovazzi ◽  
Angela Piazzi ◽  
Michele Lanotte ◽  
...  
Keyword(s):  
Stem Cells ◽  
Genetic Alterations ◽  
Tumor Stem Cells ◽  
Primary Tumors ◽  
Immunodeficient Mice ◽  
Brain Tumor Stem Cells ◽  
Tumor Phenotype ◽  
Fetal Bovine ◽  
Primary Glioblastomas

Formation of neurospheres (NS) in cultures of glioblastomas (GBMs), with self-renewal, clonogenic capacities, and tumorigenicity following transplantation into immunodeficient mice, may denounce the existence of brain tumor stem cells (BTSCs) in vivo. In sixteen cell lines from resected primary glioblastomas, NS showed the same genetic alterations as primary tumors and the expression of stemness antigens. Adherent cells (AC), after adding 10% of fetal bovine serum (FBS) to the culture, were genetically different from NS and prevailingly expressed differentiation antigens. NS developed from a highly malignant tumor phenotype with proliferation, circumscribed necrosis, and high vessel density. Beside originating from transformed neural stem cells (NSCs), BTSCs may be contained within or correspond to dedifferentiated cells after mutation accumulation, which reacquire the expression of stemness antigens.

STEM-10. UPSTREAM REGULATORS OF THE GLIOMA STEM CELL PHENOTYPE

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi23-vi23
Author(s):  
Alexandra Calinescu ◽  
Zain Sultan ◽  
McKenzie Kauss ◽  
Wajd Al-Holou ◽  
Jason Heth
Keyword(s):  
Stem Cells ◽  
Tumor Grade ◽  
Telomerase Activity ◽  
Primary Brain Tumor ◽  
Tumor Formation ◽  
High Expression ◽  
Cell Phenotype ◽  
Proliferative Potential ◽  
Loss Of Function ◽  
Significant Enrichment

Abstract Glioblastoma (GBM) is the most common and deadly primary brain tumor in adults. Recurrence of the disease is attributed in part to the presence of Glioma Stem Cells (GSC), which are resistant to chemo- and radiotherapy and can initiate tumor formation. Molecularly, GSCs resemble the mesenchymal subtype that is associated with worse prognosis. GSCs share many characteristics with Neural Stem Cells (NSCs) including proliferative potential, migratory capacity, telomerase activity, diverse progeny and similar gene signature, however differ fundamentally from NSCs in their tumor forming ability. RNA-Seq analysis of GSCs and NSCs illustrates significant enrichment in GSCs of transcription factors (TFs) known to be dysregulated in cancer, chief among them being SIX1, a developmental TF with documented roles in progression of multiple cancers. Overexpression of SIX1 in A172 GBM cells enhances proliferation, promotes resistance to radiotherapy and alters expression of a core set of 4 developmental TFs (POU3F2, SALL2, OLIG2 and SOX2) capable to reprogram differentiated GBM cells into GSCs (Suva et al., 2014). Analysis of SIX1 in surgical samples from glioma patients illustrates that high expression of SIX1 correlates with tumor grade, finding corroborated in the TCGA and CGGA data sets. Surprisingly, primary NSCs, after extended time in culture, increase their proliferation rate, acquire a mesenchymal transcriptional signature akin to GSCs, including high expression of SIX1, and form deadly tumors when implanted into the brains of mice. Comparing the epigenetic landscape of transformed and normal NSCs we identify a significant enrichment of accessible chromatin at promoter and enhancer loci in transformed NSCs, including at regulatory regions of SIX1 and of genes that define mesenchymal GBM. These data suggest that SIX1 may represent an upstream regulator of the GSC phenotype and may drive malignant transformation of NSCs. Genetic and epigenetic loss of function analyses are ongoing to test this hypothesis.

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