Mammosphere cells from high-passage MCF7 cell line show variable loss of tumorigenicity and radioresistance

Xie, Guozhu; Zhan, Junfang; Tian, Yunhong; Liu, Ying; Chen, Zhixian; Ren, Chen; Sun, Qianli; Lian, Jianping; Chen, Longhua; Ruan, Jian; Ye, Changsheng; Sun, Ai-Min; Yuan, Yawei

doi:10.1016/j.canlet.2011.10.018

Cited by 25 publications

(21 citation statements)

References 38 publications

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“…Colonies containing >50 cells were counted under a light microscope. The surviving fraction was calculated as described previously (19). In some experiments, cells were treated with LY294002 starting 1 hour before radiation for a duration of 24 hours.…”

Section: Irradiation and Clonogenic Assaymentioning

confidence: 99%

MiR-20a Induces Cell Radioresistance by Activating the PTEN/PI3K/Akt Signaling Pathway in Hepatocellular Carcinoma

Zhang

Zheng

Ding

et al. 2015

International Journal of Radiation Oncology*Biology*Physics

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Section: Irradiation and Clonogenic Assaymentioning

confidence: 99%

MiR-20a Induces Cell Radioresistance by Activating the PTEN/PI3K/Akt Signaling Pathway in Hepatocellular Carcinoma

Zhang

Zheng

Ding

et al. 2015

International Journal of Radiation Oncology*Biology*Physics

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“…It has been previously shown that the fraction of CD44 high /CD24 low cells in tumorspheres is significantly elevated compared to classical monolayer cell cultures [32,45,46]. This fact solves the technical problems associated with rare cell studies [47].…”

Section: Discussionmentioning

confidence: 99%

Kinetics of MDR Transport in Tumor-Initiating Cells

2013

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Multidrug resistance (MDR) driven by ABC (ATP binding cassette) membrane transporters is one of the major causes of treatment failure in human malignancy. MDR capacity is thought to be unevenly distributed among tumor cells, with higher capacity residing in tumor-initiating cells (TIC) (though opposite finding are occasionally reported). Functional evidence for enhanced MDR of TICs was previously provided using a “side population” assay. This assay estimates MDR capacity by a single parameter - cell’s ability to retain fluorescent MDR substrate, so that cells with high MDR capacity (“side population”) demonstrate low substrate retention. In the present work MDR in TICs was investigated in greater detail using a kinetic approach, which monitors MDR efflux from single cells. Analysis of kinetic traces obtained allowed for the estimation of both the velocity (V max) and affinity (K M) of MDR transport in single cells. In this way it was shown that activation of MDR in TICs occurs in two ways: through the increase of V max in one fraction of cells, and through decrease of K M in another fraction. In addition, kinetic data showed that heterogeneity of MDR parameters in TICs significantly exceeds that of bulk cells. Potential consequences of these findings for chemotherapy are discussed.

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“…Cancer stem cells are postulated to be involved in the generation of primary breast tumors and their progression to undifferentiated tumors and metastasis, and are claimed to be enriched within mammospheres (34,35). Although ethanol affects the proliferation and differentiation of normal embryonic and adult stem cells (36,37), it is not known whether it activates and/or increases the number of cancer stem cells.…”

Section: Introductionmentioning

confidence: 99%

Long-term exposure of MCF-7 breast cancer cells to ethanol stimulates oncogenic features

Gelfand

Vernet

Bruhn

et al. 2016

International Journal of Oncology

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Alcohol consumption is a risk factor for breast cancer. Little is known regarding the mechanism, although it is assumed that acetaldehyde or estrogen mediated pathways play a role. We previously showed that long-term exposure to 2.5 mM ethanol (blood alcohol ~0.012%) of MCF-12A, a human normal epithelial breast cell line, induced epithelial mesenchymal transition (EMT) and oncogenic transformation. In this study, we investigated in the human breast cancer cell line MCF-7, whether a similar exposure to ethanol at concentrations ranging up to peak blood levels in heavy drinkers would increase malignant progression. Short-term (1-week) incubation to ethanol at as low as 1–5 mM (corresponding to blood alcohol concentration of ~0.0048–0.024%) upregulated the stem cell related proteins Oct4 and Nanog, but they were reduced after exposure at 25 mM. Long-term (4-week) exposure to 25 mM ethanol upregulated the Oct4 and Nanog proteins, as well as the malignancy marker Ceacam6. DNA microarray analysis in cells exposed for 1 week showed upregulated expression of metallothionein genes, particularly MT1X. Long-term exposure upregulated expression of some malignancy related genes (STEAP4, SERPINA3, SAMD9, GDF15, KRT15, ITGB6, TP63, and PGR, as well as the CEACAM, interferon related, and HLA gene families). Some of these findings were validated by RT-PCR. A similar treatment also modulated numerous microRNAs (miRs) including one regulator of Oct4 as well as miRs involved in oncogenesis and/or malignancy, with only a few estrogen-induced miRs. Long-term 25 mM ethanol also induced a 5.6-fold upregulation of anchorage-independent growth, an indicator of malignant-like features. Exposure to acetaldehyde resulted in little or no effect comparable to that of ethanol. The previously shown alcohol induction of oncogenic transformation of normal breast cells is now complemented by the current results suggesting alcohol's potential involvement in malignant progression of breast cancer.

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Mammosphere cells from high-passage MCF7 cell line show variable loss of tumorigenicity and radioresistance

Cited by 25 publications

References 38 publications

MiR-20a Induces Cell Radioresistance by Activating the PTEN/PI3K/Akt Signaling Pathway in Hepatocellular Carcinoma

MiR-20a Induces Cell Radioresistance by Activating the PTEN/PI3K/Akt Signaling Pathway in Hepatocellular Carcinoma

Kinetics of MDR Transport in Tumor-Initiating Cells

Long-term exposure of MCF-7 breast cancer cells to ethanol stimulates oncogenic features

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