scholarly journals Do cancer cells undergo phenotypic switching? The case for imperfect cancer stem cell markers

2012 ◽  
Vol 2 (1) ◽  
Author(s):  
Stefano Zapperi ◽  
Caterina A. M. La Porta
Keyword(s):  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Phenotypic Switching ◽  
Stem Cell Markers ◽  
Cell Markers ◽  
Cancer Stem Cell Markers

scholarly journals DSPP-MMP20 gene silencing downregulates cancer stem cell markers in human oral cancer cells

2018 ◽  
Vol 23 (1) ◽  
Author(s):  
Nikolaos G. Nikitakis ◽  
Ioannis Gkouveris ◽  
Jaya Aseervatham ◽  
Kelvin Barahona ◽  
Kalu U. E. Ogbureke
Keyword(s):  
Stem Cell ◽  
Oral Cancer ◽  
Cancer Stem Cell ◽  
Gene Silencing ◽  
Cancer Cells ◽  
Stem Cell Markers ◽  
Cell Markers ◽  
Cancer Stem Cell Markers ◽  
Oral Cancer Cells

scholarly journals Cancer-Associated Fibroblasts Regulate the Plasticity of Breast Cancer Stemness through the Production of Leukemia Inhibitory Factor

Life ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1298
Author(s):  
Nazanin Vaziri ◽  
Laleh Shariati ◽  
Ali Zarrabi ◽  
Ali Farazmand ◽  
Shaghayegh Haghjooy Javanmard
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Leukemia Inhibitory Factor ◽  
Breast Cancer Cells ◽  
Stem Cell Markers ◽  
Cancer Associated Fibroblasts ◽  
Cell Markers ◽  
Cancer Stem Cell Markers

Leukemia inhibitory factor (LIF), as a member of the interleukin-6 cytokine family, plays a complex role in solid tumors. However, the effect of LIF as a tumor microenvironment factor on plasticity control in breast cancer remains largely unknown. In this study, an in vitro investigation is conducted to determine the crosstalk between breast cancer cells and fibroblasts. Based on the results, cancer-associated fibroblasts are producers of LIF in the cocultivation system with breast cancer cells. Treatment with the CAF-CM and human LIF protein significantly promoted stemness through the dedifferentiation process and regaining of stem-cell-like properties. In addition, the results indicate that activation of LIFR signaling in breast cancer cells in the existence of CAF-secreted LIF can induce Nanog and Oct4 expression and increase breast cancer stem cell markers CD24−/CD44+. In contrast, suppression of the LIF receptor by human LIF receptor inhibition antibody decreased the cancer stem cell markers. We found that LIF was frequently overexpressed by CAFs and that LIF expression is necessary for dedifferentiation of breast cancer cell phenotype and regaining of cancer stem cell properties. Our results suggest that targeting LIF/LIFR signaling might be a potent therapeutic strategy for breast cancer and the prevention of tumor recurrence.

scholarly journals Evaluation of Cancer Stem Cell Markers CD133, CD44, CD24: Association with AKT Isoforms and Radiation Resistance in Colon Cancer Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e94621 ◽  
Author(s):  
Sara Häggblad Sahlberg ◽  
Diana Spiegelberg ◽  
Bengt Glimelius ◽  
Bo Stenerlöw ◽  
Marika Nestor
Keyword(s):  
Colon Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Radiation Resistance ◽  
Stem Cell Markers ◽  
Colon Cancer Cells ◽  
Cell Markers ◽  
Cancer Stem Cell Markers ◽  
Akt Isoforms

scholarly journals The Significance of Cancer Stem Cell Markers’ Gene Expression and Relevance for Survival Outcomes

2020 ◽  
Author(s):  
Kevin Dzobo ◽  
Dimakatso Senthebane ◽  
Chelene Ganz ◽  
Nicholas Thomford
Keyword(s):  
Gene Expression ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Therapy Resistance ◽  
Stem Cell Markers ◽  
Cancer Drugs ◽  
Cell Markers ◽  
Cancer Stem Cell Markers ◽  
New Findings

Solid tumors display complex biology and most therapies including chemotherapy cannot prevent therapy resistance and relapse. Most therapeutics target cancer cells, but recent data suggest the presence of cancer stem cells as cells with self-renewal and tumorigenic abilities. Cancer stem cell markers have been suggested to have prognostic value and can be targeted during cancer treatment and in resistant disease. CSCs have been postulated to play significant contextual roles in tumor initiation, progression, therapy resistance and metastasis. CSCs have thus been targeted by new generation cancer drugs. The transcriptional expression of several CSC markers in different cancers was evaluated by searching publicly available The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA) databases. We report here new findings on expression and prognostic significance of CSC markers in several cancers by examining the expression of CSCs markers in tumor tissues versus the adjacent normal tissues. We found that CSC markers were mostly highly expressed various tumors such as colon, lung, pancreatic and esophageal cancers. No CSC marker is expressed in the same pattern in all cancers and individual CSC marker expression was not linked to patient survival. This analysis calls for continued research on CSCs and clinical evaluation of the CSC markers in relation to prognosis of cancers in large population samples. Novel cancer drugs ought to target CSCs, cancer cells and tumor microenvironment variations.

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