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Article

Alternative lengthening of telomeres is induced by telomerase inhibitors in Barrett's esophageal cells

  • Authors:
    • Xiuguang Qin
    • Bo Qi
    • Baosheng Zhao
  • View Affiliations / Copyright

    Affiliations: Department of Thoracic Surgery, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China
  • Pages: 1399-1404
    |
    Published online on: January 17, 2013
       https://doi.org/10.3892/or.2013.2238
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Abstract

A crucial step in the path to the malignant transformation of cells and tumor formation is immortalization, which essentially depends on telomere maintenance. The aim of this study was to investigate the role of telomerase in the progression of Barrett's esophagus. Telomerase activity was measured in Barrett's cells using terminal restriction fragment (TRF) analysis. Telomere length was measured using Q-FISH analysis. Furthermore, the telomere recombination events were detected between sister chromatids using chromosome orientation FISH (CO-FISH). There was a reduction in telomerase activity in the CP-A cells transduced with MT-hTER/47A+siRNA, which led to an almost complete disappearance of telomerase activity. The telomere length of the CP-A cells transduced with MT-hTER/47A+siRNA was slightly shorter compared to that of the untransduced cells. The telomerase-inhibited cells were morphologically indistinguishable from those untransduced and WT-hter-transduced cells. In the control cells, the growth rate was between 0.9 to 1.1 with the population doubling per day. Although the transduction of the telomerase inhibitors in the CP-A cells did not cause a significant reduction in cell growth, these transduced cells grew generally slower compared with the control cells. The heterogeneous telomere length was also be detected in the telomerase-inhibited CP-A cells. However, the telomere length remained homogeneous in the control cells. The metaphase of the CP-A cells transduced with MT-hTER/47A+siRNA demonstrated 70% heterogeneous telomeres. In addition, no increased recombination was observed between sister chromatids in the transduced CP-A cells compared with the control cells. Our findings suggest that an alternative lengthening of telomeres (ALT) may be induced by telomerase inhibitors in CP-A cells. Therefore, telomerase inhibitors may exhibit high potency in the treatment of esophageal adenocarcinoma arising from Barrett's esophagus.
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Copy and paste a formatted citation
Spandidos Publications style
Qin X, Qi B and Zhao B: Alternative lengthening of telomeres is induced by telomerase inhibitors in Barrett's esophageal cells. Oncol Rep 29: 1399-1404, 2013.
APA
Qin, X., Qi, B., & Zhao, B. (2013). Alternative lengthening of telomeres is induced by telomerase inhibitors in Barrett's esophageal cells. Oncology Reports, 29, 1399-1404. https://doi.org/10.3892/or.2013.2238
MLA
Qin, X., Qi, B., Zhao, B."Alternative lengthening of telomeres is induced by telomerase inhibitors in Barrett's esophageal cells". Oncology Reports 29.4 (2013): 1399-1404.
Chicago
Qin, X., Qi, B., Zhao, B."Alternative lengthening of telomeres is induced by telomerase inhibitors in Barrett's esophageal cells". Oncology Reports 29, no. 4 (2013): 1399-1404. https://doi.org/10.3892/or.2013.2238
Copy and paste a formatted citation
x
Spandidos Publications style
Qin X, Qi B and Zhao B: Alternative lengthening of telomeres is induced by telomerase inhibitors in Barrett's esophageal cells. Oncol Rep 29: 1399-1404, 2013.
APA
Qin, X., Qi, B., & Zhao, B. (2013). Alternative lengthening of telomeres is induced by telomerase inhibitors in Barrett's esophageal cells. Oncology Reports, 29, 1399-1404. https://doi.org/10.3892/or.2013.2238
MLA
Qin, X., Qi, B., Zhao, B."Alternative lengthening of telomeres is induced by telomerase inhibitors in Barrett's esophageal cells". Oncology Reports 29.4 (2013): 1399-1404.
Chicago
Qin, X., Qi, B., Zhao, B."Alternative lengthening of telomeres is induced by telomerase inhibitors in Barrett's esophageal cells". Oncology Reports 29, no. 4 (2013): 1399-1404. https://doi.org/10.3892/or.2013.2238
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