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Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...

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Related Experiment Video

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Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
08:46

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Developing multidrug-resistant cells and exploring correlation between BCRP/ABCG2 over-expression and DNA

Nana Ji1, Jianhui Yuan, Jianjun Liu

  • 1Shenzhen University, China.

Acta Biochimica Et Biophysica Sinica
|November 26, 2010
PubMed
Summary

Multidrug resistance in cancer cells is often caused by breast cancer resistance protein (BCRP/ABCG2) overexpression, which reduces chemotherapy drug accumulation. This study links BCRP/ABCG2 upregulation to decreased DNA methyltransferases, particularly DNMT3b, in resistant cells.

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Breast cancer resistance protein/ATP-binding cassette sub-family G member 2 (BCRP/ABCG2) expression is a key factor in chemotherapy failure.
  • Understanding multidrug resistance mechanisms is crucial for effective cancer treatment.

Purpose of the Study:

  • To develop and characterize multidrug-resistant cells overexpressing BCRP/ABCG2.
  • To investigate the relationship between BCRP/ABCG2 expression, drug accumulation, and DNA methyltransferase levels.

Main Methods:

  • Development of mitoxantrone-resistant MCF-7 cells.
  • Analysis of BCRP/ABCG2 mRNA and protein via real-time PCR and Western blot.
  • Assessment of intracellular drug accumulation using flow cytometry.
  • Evaluation of DNA methyltransferase expression by Western blot.

Main Results:

  • Mitoxantrone-resistant cells showed cross-resistance to adriamycin and taxol.
  • BCRP/ABCG2 mRNA and protein levels increased with mitoxantrone resistance.
  • Intracellular mitoxantrone accumulation decreased as BCRP/ABCG2 expression rose.
  • Significant decrease in DNA methyltransferase 3b (DNMT3b) expression was observed.

Conclusions:

  • Overexpression of BCRP/ABCG2 and its drug-efflux activity are primary drivers of multidrug resistance.
  • Multidrug resistance is associated with BCRP/ABCG2 upregulation and reduced DNA methyltransferase expression, especially DNMT3b.