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International Journal of Oncology
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Print ISSN: 1019-6439 Online ISSN: 1791-2423
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May-2015 Volume 46 Issue 5

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International Journal of Molecular Medicine

International Journal of Molecular Medicine

International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

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International Journal of Oncology

International Journal of Oncology is an international journal devoted to oncology research and cancer treatment.

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Molecular Medicine Reports

Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery.

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Oncology Reports is an international journal devoted to fundamental and applied research in Oncology.

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Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine.

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Oncology Letters is an international journal devoted to Experimental and Clinical Oncology.

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Explores a wide range of biological and medical fields, including pharmacology, genetics, microbiology, neuroscience, and molecular cardiology.

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International journal addressing all aspects of oncology research, from tumorigenesis and oncogenes to chemotherapy and metastasis.

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Multidisciplinary open-access journal spanning biochemistry, genetics, neuroscience, environmental health, and synthetic biology.

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International Journal of Functional Nutrition

Open-access journal combining biochemistry, pharmacology, immunology, and genetics to advance health through functional nutrition.

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International Journal of Epigenetics

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Article

Inhibition of the transient receptor potential melastatin-2 channel causes increased DNA damage and decreased proliferation in breast adenocarcinoma cells

  • Authors:
    • Mandi M. Hopkins
    • Xiaoxing Feng
    • Mengwei Liu
    • Lauren P. Parker
    • David W. Koh
  • View Affiliations / Copyright

    Affiliations: Department of Pharmaceutical Sciences, Washington State University, Pullman, WA 99164, USA, Department of Pharmaceutical and Biomedical Sciences, Ohio Northern University, Ada, OH 45810, USA
  • Pages: 2267-2276
    |
    Published online on: March 6, 2015
       https://doi.org/10.3892/ijo.2015.2919
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Abstract

Transient receptor potential, melastatin-2 (TRPM2) is a plasma membrane cation channel with important roles in sensory functions and promoting cell death. However, we demonstrated here that TRPM2 was present in the nuclei of MCF-7 and MDA-MB-231 human breast adenocarcinoma cells, and its pharmacologic inhibition or RNAi silencing caused decreased cell proliferation. Neither an effect on proliferation nor a localization of TRPM2 in the nucleus was observed in noncancerous HMEC and MCF-10A human mammary epithelial cells. Investigation of possible effects of TRPM2 function in the nucleus demonstrated that pharmacologic inhibition or RNAi silencing of TRPM2 in MCF-7 and MDA-MB-231 human breast adenocarcinoma cells caused up to 4-fold increases in DNA damage levels, as compared to noncancerous breast cells after equivalent treatments. These results indicate that TRPM2 has a novel nuclear function in human breast adenocarcinoma cells that facilitates the integrity of genomic DNA, a finding that is distinct from its previously reported role as a plasma membrane cation channel in noncancerous cells. In summary, we report here a novel effect promoted by TRPM2, where it functions to minimize DNA damage and thus may have a role in the protection of genomic DNA in breast cancer cells. Our study therefore provides compelling evidence that TRPM2 has a unique role in breast adenocarcinoma cells. Accordingly, these studies suggest that TRPM2 is a potential therapeutic target, where its pharmacologic inhibition may provide an innovative strategy to selectively increase DNA damage levels in breast cancer cells.
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Copy and paste a formatted citation
Spandidos Publications style
Hopkins MM, Feng X, Liu M, Parker LP and Koh DW: Inhibition of the transient receptor potential melastatin-2 channel causes increased DNA damage and decreased proliferation in breast adenocarcinoma cells. Int J Oncol 46: 2267-2276, 2015.
APA
Hopkins, M.M., Feng, X., Liu, M., Parker, L.P., & Koh, D.W. (2015). Inhibition of the transient receptor potential melastatin-2 channel causes increased DNA damage and decreased proliferation in breast adenocarcinoma cells. International Journal of Oncology, 46, 2267-2276. https://doi.org/10.3892/ijo.2015.2919
MLA
Hopkins, M. M., Feng, X., Liu, M., Parker, L. P., Koh, D. W."Inhibition of the transient receptor potential melastatin-2 channel causes increased DNA damage and decreased proliferation in breast adenocarcinoma cells". International Journal of Oncology 46.5 (2015): 2267-2276.
Chicago
Hopkins, M. M., Feng, X., Liu, M., Parker, L. P., Koh, D. W."Inhibition of the transient receptor potential melastatin-2 channel causes increased DNA damage and decreased proliferation in breast adenocarcinoma cells". International Journal of Oncology 46, no. 5 (2015): 2267-2276. https://doi.org/10.3892/ijo.2015.2919
Copy and paste a formatted citation
x
Spandidos Publications style
Hopkins MM, Feng X, Liu M, Parker LP and Koh DW: Inhibition of the transient receptor potential melastatin-2 channel causes increased DNA damage and decreased proliferation in breast adenocarcinoma cells. Int J Oncol 46: 2267-2276, 2015.
APA
Hopkins, M.M., Feng, X., Liu, M., Parker, L.P., & Koh, D.W. (2015). Inhibition of the transient receptor potential melastatin-2 channel causes increased DNA damage and decreased proliferation in breast adenocarcinoma cells. International Journal of Oncology, 46, 2267-2276. https://doi.org/10.3892/ijo.2015.2919
MLA
Hopkins, M. M., Feng, X., Liu, M., Parker, L. P., Koh, D. W."Inhibition of the transient receptor potential melastatin-2 channel causes increased DNA damage and decreased proliferation in breast adenocarcinoma cells". International Journal of Oncology 46.5 (2015): 2267-2276.
Chicago
Hopkins, M. M., Feng, X., Liu, M., Parker, L. P., Koh, D. W."Inhibition of the transient receptor potential melastatin-2 channel causes increased DNA damage and decreased proliferation in breast adenocarcinoma cells". International Journal of Oncology 46, no. 5 (2015): 2267-2276. https://doi.org/10.3892/ijo.2015.2919
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