We are analyzing https://link.springer.com/article/10.1186/bcr2583.

Title:
Senescence evasion by MCF-7 human breast tumor-initiating cells | Breast Cancer Research
Description:
Introduction A subpopulation of cancer cells, tumor-initiating cells, is believed to be the driving force behind tumorigenesis and resistance to radiation and chemotherapy. The persistence of tumor-initiating cells may depend on altered regulation of DNA damage and checkpoint proteins, as well as a reduced propensity to undergo apoptosis or senescence. Methods To test this hypothesis, we isolated CD24-/low/CD44+ tumor-initiating cells (as mammospheres) from MCF-7 breast cancer cells grown in adherent monolayer culture, and carried out a comprehensive comparison of cell death and DNA damage response pathways prior to and after exposure to ionizing radiation in mammospheres and monolayer MCF-7 cells. Single and double-strand break repair was measured by single-cell gel electrophoresis. The latter was also examined by phosphorylation of histone H2AX and formation of 53BP1 and Rad51 foci. Apoptosis was quantified by flow-cytometric analysis of annexin V-binding and senescence was analyzed on the basis of cellular β-galactosidase activity. We employed the telomeric repeat amplification protocol to quantify telomerase activity. Expression of key DNA repair and cell cycle regulatory proteins was detected and quantified by western blot analysis. Results Our data demonstrate that in comparison to the bulk population of MCF-7 cells (predominantly CD24+/CD44+), the MCF-7 mammosphere cells benefit from a multifaceted approach to cellular protection relative to that seen in monolayer cells, including a reduced level of reactive oxygen species, a more active DNA single-strand break repair (SSBR) pathway, possibly due to a higher level of expression of the key SSBR protein, human AP endonuclease 1 (Ape1), and a significantly reduced propensity to undergo senescence as a result of increased telomerase activity and a low level of p21 protein expression. No significant difference was seen in the rates of double-strand break repair (DSBR) between the two cell types, but DSBR in mammospheres appears to by-pass the need for H2AX phosphorylation. Conclusions Enhanced survival of MCF-7 tumor-initiating cells in response to ionizing radiation is primarily dependent on an inherent down-regulation of the senescence pathway. Since MCF-7 cells are representative of cancer cells that do not readily undergo apoptosis, consideration of senescence pathways may play a role in targeting stem cells from such tumors.
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Keywords {🔍}

cells, cell, cancer, article, pubmed, mammospheres, google, scholar, monolayer, cas, mcf, stem, usa, dna, senescence, repair, expression, breast, phosphorylation, mammosphere, radiation, figure, unirradiated, response, damage, proteins, activity, telomerase, protein, assay, apoptosis, level, hax, chk, analysis, human, ionizing, population, survival, irradiated, data, pathway, irradiation, cycle, minutes, authors, types, γradiation, control, file,

Topics {✒️}

r-phycoerythrin-labelled anti-cd24 real-time quantitative rt-pcr fitc-labelled anti-cd44 antibodies cd24-/low/cd44+ expression compared cd24-/low/cd44+ mcf-7 cells phycoerythrin-labelled anti-cd24 xrcc1/dna ligase iii quantitative rt-pcr assay dna-activated protein kinase double-strand break repair uv-induced dna damage single-strand break repair double-stranded-break repair mcf-7 tumor-initiating cells tumor-initiating cells isolated rad51 focus formation article download pdf progenitor/stem cells derived mcf-7 cancer-initiating cells cellular β-galactosidase activity radiation-induced strand breaks stem/progenitor cell properties human mammary gland double-strand break formation annexin v-fitc binding dna damage/cell cycle dmem/f12 medium supplemented propidium iodide/rnase solution single-cell gel electrophoresis ros-induced dna damage serum-free medium supplemented induce stress-induced premature article karimi-busheri anti-rad51mouse monoclonal antibody anti-phospho-histone h2ax quantitative rt-pcr research triangle park phospho-dna-pkcs refer radiation-induced cell death radiation-induced telomerase activity adenovirus-mediated p16ink4a expression renewing tumor-initiating susan lees-miller polyclonal anti-ku80 antibody double-strand breaks full size image tumor-initiating cells reactive oxygen species distinct molecular signature telomerase-extended primer appears

Questions {❓}

Dumitrescu RG, Cotarla I: Understanding breast cancer risk -- where do we stand in 2005?

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WebPage:
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         headline:Senescence evasion by MCF-7 human breast tumor-initiating cells
         description:A subpopulation of cancer cells, tumor-initiating cells, is believed to be the driving force behind tumorigenesis and resistance to radiation and chemotherapy. The persistence of tumor-initiating cells may depend on altered regulation of DNA damage and checkpoint proteins, as well as a reduced propensity to undergo apoptosis or senescence. To test this hypothesis, we isolated CD24-/low/CD44+ tumor-initiating cells (as mammospheres) from MCF-7 breast cancer cells grown in adherent monolayer culture, and carried out a comprehensive comparison of cell death and DNA damage response pathways prior to and after exposure to ionizing radiation in mammospheres and monolayer MCF-7 cells. Single and double-strand break repair was measured by single-cell gel electrophoresis. The latter was also examined by phosphorylation of histone H2AX and formation of 53BP1 and Rad51 foci. Apoptosis was quantified by flow-cytometric analysis of annexin V-binding and senescence was analyzed on the basis of cellular β-galactosidase activity. We employed the telomeric repeat amplification protocol to quantify telomerase activity. Expression of key DNA repair and cell cycle regulatory proteins was detected and quantified by western blot analysis. Our data demonstrate that in comparison to the bulk population of MCF-7 cells (predominantly CD24+/CD44+), the MCF-7 mammosphere cells benefit from a multifaceted approach to cellular protection relative to that seen in monolayer cells, including a reduced level of reactive oxygen species, a more active DNA single-strand break repair (SSBR) pathway, possibly due to a higher level of expression of the key SSBR protein, human AP endonuclease 1 (Ape1), and a significantly reduced propensity to undergo senescence as a result of increased telomerase activity and a low level of p21 protein expression. No significant difference was seen in the rates of double-strand break repair (DSBR) between the two cell types, but DSBR in mammospheres appears to by-pass the need for H2AX phosphorylation. Enhanced survival of MCF-7 tumor-initiating cells in response to ionizing radiation is primarily dependent on an inherent down-regulation of the senescence pathway. Since MCF-7 cells are representative of cancer cells that do not readily undergo apoptosis, consideration of senescence pathways may play a role in targeting stem cells from such tumors.
         datePublished:2010-06-02T00:00:00Z
         dateModified:2010-06-02T00:00:00Z
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            Cancer Stem Cell
            Replicative Senescence
            Telomeric Repeat Amplification Protocol
            H2AX Phosphorylation
            Rad51 Focus
            Cancer Research
            Oncology
            Surgical Oncology
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      headline:Senescence evasion by MCF-7 human breast tumor-initiating cells
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      keywords:
         Cancer Stem Cell
         Replicative Senescence
         Telomeric Repeat Amplification Protocol
         H2AX Phosphorylation
         Rad51 Focus
         Cancer Research
         Oncology
         Surgical Oncology
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               type:PostalAddress
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      name:NovaRx Corporation, Stem Cell Program, San Diego, USA
      name:Department of Oncology, University of Alberta and Department of Experimental Oncology, Cross Cancer Institute, Edmonton, Canada
      name:Department of Oncology, University of Alberta and Department of Experimental Oncology, Cross Cancer Institute, Edmonton, Canada
      name:Department of Oncology, University of Alberta and Department of Experimental Oncology, Cross Cancer Institute, Edmonton, Canada

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