Alterations in nuclear pore architecture allow cancer cell entry into or exit from drug-resistant dormancy.
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Publication Details
Output type: Journal article
Author list: Kinoshita, Kalir, Rahaman, Dottino, Kohtz
Publisher: Elsevier
Publication year: 2012
Volume number: 180
Issue number: 1
Start page: 375
End page: 89
Number of pages: -285
ISSN: 0002-9440
eISSN: 1525-2191
Languages: English-Great Britain (EN-GB)
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Open access status: hybrid
Full text URL: http://ajp.amjpathol.org/article/S000294401100914X/pdf
Abstract
Phenotypic diversity arises in tumors just as it does in developing organisms, and tumor recurrence frequently manifests from the selective survival of divergent drug-resistant cells. Although the expanding tumor cell population may be successfully targeted, drug-resistant cells may persist and sustain the tumor or enter dormancy before igniting a future relapse. Herein, we show that partial knockdown of nucleoporin p62 (NUP62) by small-interfering RNA confers cisplatin resistance to cultured high-grade ovarian carcinoma cells. Treatment with NUP62 small-interfering RNA and cisplatin leaves resistant cells in a state of dormancy; some dormant cells can be induced to proliferate by transient induction of NUP62 expression from an ectopic expression construct. In addition to suggesting functional links between nuclear pore complex architecture and cancer cell survival, the culture system provides a novel experimental window into the dynamics of tumor cell drug resistance and dormancy.
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