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Abstract C65: Drug-tolerant cancer cells show reduced tumor-initiating capacity: Depletion of CD44+ cells and evidence for epigenetic mechanisms

Xin Chen, Izabela Fokt, Stanislaw Skora, Waldemar Priebe, Yongyi Bi, Dean G. Tang, Hong Yan, Qiuping Zhang, Jichao Qin, Hangwen Li, Can Liu, Tammy Davis, Luis D. Coletta and Jim Klostergaard
Xin Chen
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Izabela Fokt
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Stanislaw Skora
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Waldemar Priebe
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Yongyi Bi
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Dean G. Tang
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Hong Yan
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Qiuping Zhang
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Jichao Qin
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Hangwen Li
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Can Liu
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Tammy Davis
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Luis D. Coletta
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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Jim Klostergaard
University of Texas MD Anderson Cancer Center, Smithville, TX, Universtiy of Texas MD Anderson Cancer Center, Houston, TX, Wuhan University School of Public Health, Wuhan, Hubei, China, Wuhan University School of Basic Medical Science, Wuhan, Hubei, China, Tongji Hospital, Wuhan, Hubei, China, The Methodist Hospital, Houston, TX
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DOI: 10.1158/1538-7445.PRCA2012-C65 Published February 2012
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Abstract

Cancer stem cells (CSCs) possess high tumor-initiating capacity and have been reported to be resistant to therapeutics. Vice versa, therapy-resistant cancer cells seem to manifest CSC phenotypes and properties. It has been generally assumed that drug-resistant cancer cells may all be CSCs although the generality of this assumption is unknown. Here, we chronically treated Du145 prostate cancer cells with etoposide, paclitaxel and some experimental drugs (i.e., staurosporine and 2 paclitaxel analogs), which led to populations of drug-tolerant cells (DTCs). Surprisingly, these DTCs, when implanted either subcutaneously or orthotopically into NOD/SCID mice, exhibited much reduced tumorigenicity or were even nontumorigenic. Drug-tolerant DLD1 colon cancer cells selected by a similar chronic selection protocol also displayed reduced tumorigenicity whereas drug-tolerant UC14 bladder cancer cells demonstrated either increased or decreased tumor-regenerating capacity. Drug-tolerant Du145 cells demonstrated low proliferative and clonogenic potential and were virtually devoid of CD44+ cells. Prospective knockdown of CD44 in Du145 cells inhibited cell proliferation and tumor regeneration whereas restoration of CD44 expression in drug-tolerant Du145 cells increased cell proliferation and partially increased tumorigenicity. Interestingly, drug-tolerant Du145 cells showed both increases and decreases in many ‘stemness’ genes. Finally, evidence was provided that chronic drug exposure generated DTCs via epigenetic mechanisms involving molecules such as CD44 and KDM5A. Our results thus reveal that 1) not all DTCs are necessarily CSCs; 2) conventional chemotherapeutic drugs such as taxol and etoposide may directly target CD44+ tumor-initiating cells; and 3) DTCs generated via chronic drug selection involve epigenetic mechanisms.

Citation Format: Xin Chen, Izabela Fokt, Stanislaw Skora, Waldemar Priebe, Yongyi Bi, Dean G. Tang, Hong Yan, Qiuping Zhang, Jichao Qin, Hangwen Li, Can Liu, Tammy Davis, Luis D. Coletta, Jim Klostergaard. Drug-tolerant cancer cells show reduced tumor-initiating capacity: Depletion of CD44+ cells and evidence for epigenetic mechanisms [abstract]. In: Proceedings of the AACR Special Conference on Advances in Prostate Cancer Research; 2012 Feb 6-9; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2012;72(4 Suppl):Abstract nr C65.

  • ©2012 American Association for Cancer Research.
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Cancer Research: 72 (4 Supplement)
February 2012
Volume 72, Issue 4 Supplement
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Abstract C65: Drug-tolerant cancer cells show reduced tumor-initiating capacity: Depletion of CD44+ cells and evidence for epigenetic mechanisms
Xin Chen, Izabela Fokt, Stanislaw Skora, Waldemar Priebe, Yongyi Bi, Dean G. Tang, Hong Yan, Qiuping Zhang, Jichao Qin, Hangwen Li, Can Liu, Tammy Davis, Luis D. Coletta and Jim Klostergaard
Cancer Res February 6 2012 (72) (4 Supplement) C65; DOI: 10.1158/1538-7445.PRCA2012-C65

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Abstract C65: Drug-tolerant cancer cells show reduced tumor-initiating capacity: Depletion of CD44+ cells and evidence for epigenetic mechanisms
Xin Chen, Izabela Fokt, Stanislaw Skora, Waldemar Priebe, Yongyi Bi, Dean G. Tang, Hong Yan, Qiuping Zhang, Jichao Qin, Hangwen Li, Can Liu, Tammy Davis, Luis D. Coletta and Jim Klostergaard
Cancer Res February 6 2012 (72) (4 Supplement) C65; DOI: 10.1158/1538-7445.PRCA2012-C65
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Proffered Abstracts

  • Abstract 33: Interplay of DNA damage and cell cycle signaling on Replication Protein A in human cells
  • Abstract 31: Li-Fraumeni syndrome patient-derived LFS50 progression cell series: An experimental model for breast cancer prevention research
  • Abstract 32: Suppression of medical radiation DNA damage in cancer susceptible and normal humans using a new aminothiol radioprotector
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Stem Cells

  • Abstract C3: Gene expression profiling supports the hypothesis that human ovarian surface epithelia are pluripotent and capable of serving as ovarian cancer initiating cells
  • Abstract C13: Targeting interleukin 6 signaling suppresses glioma stem cell survival and tumor growth
  • Abstract C9: An in vitro model of osteoblastic bone metastasis in prostate cancer
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