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ABCG2 expression, function, and promoter methylation in human multiple myeloma.

Joel G Turner¹, Jana L Gump, Chunchun Zhang

¹H. Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Dr, Tampa, FL 33612, USA.

|August 19, 2006

Summary

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The breast cancer resistance protein (BCRP/ABCG2) is active in multiple myeloma cells and its expression increases with chemotherapy. Promoter methylation regulates BCRP/ABCG2, potentially contributing to drug resistance.

Area of Science:

Oncology
Molecular Biology
Pharmacology

Background:

The breast cancer resistance protein (BCRP/ABCG2) is implicated in multidrug resistance.
Its role in multiple myeloma (MM) drug resistance requires further elucidation.

Purpose of the Study:

To investigate the expression, function, and regulation of BCRP/ABCG2 in multiple myeloma cells.
To determine if BCRP/ABCG2 contributes to intrinsic drug resistance in MM.

Main Methods:

Quantitative PCR and Western blot for ABCG2 mRNA and protein expression.
Flow cytometry to assess drug efflux and ABCG2 function with inhibitor tryprostatin A.
Bisulfite sequencing to analyze ABCG2 promoter methylation.

Main Results:

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BCRP/ABCG2 expression increased in MM cell lines upon exposure to topotecan and doxorubicin.
Elevated ABCG2 expression was observed in MM patients post-treatment and at relapse.
BCRP/ABCG2 expression is regulated by promoter methylation and influenced by cell density.
Demethylation led to increased ABCG2 expression, confirming its functional role.

Conclusions:

BCRP/ABCG2 is expressed and functional in human myeloma cells.
Promoter methylation is a key regulatory mechanism for ABCG2 in MM.
BCRP/ABCG2 upregulation in response to chemotherapy may contribute to intrinsic drug resistance in multiple myeloma.