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Circumventing Multidrug Resistance in Cancer by ß-Galactoside Binding Protein, an Antiproliferative Cytokine

¹ Department of Chemical Biology, Laboratory for Cancer Research, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, New Jersey and ² Cell Signalling and Growth Laboratory, Division of Pharmaceutical Sciences, School of Health and Life Sciences, King's College London, Waterloo Campus, London, United Kingdom

Requests for reprints: Khew-Voon Chin, Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers University, 164 Frelinghuysen Road, Piscataway, NJ 08854. Phone: 732-445-3400; Fax: 1-732-445-0687; E-mail: chinkv{at}rci.rutgers.edu or Livio Mallucci, Cell Signalling and Growth Laboratory, Division of Pharmaceutical Sciences, School of Health and Life Sciences, King's College London, Waterloo Campus, London SE1 9NN, United Kingdom; E-mail: livio.mallucci{at}kcl.ac.uk.

We report here that ß-galactoside binding protein (ßGBP), an antiproliferative cytokine which can program cancer cells to undergo apoptosis, exhibits equal therapeutic efficacy against cancer cells that display diverse mechanisms of drug resistance and against their parental cells. The mechanisms of drug resistance in the cancer cells that we have examined include overexpression of P-glycoprotein, increased efficiency of DNA repair, and altered expression and mutation in the topoisomerase I and II enzymes. We also report that ßGBP exerted its effect by arresting the cells in S phase prior to the activation of programmed cell death. The uniquely similar profile of response to ßGBP by these drug-resistant cells and their parental cells extends the therapeutic potential of this cytokine in the treatment of cancers and offers a promising alternative to patients whose tumors are refractory to the currently available cadre of chemotherapeutic agents.

Key Words: cancer • drug resistance • ß-galactoside binding protein • ßGBP cytokine • biological therapy

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