Tetramethylpyrazine reverses multidrug resistance in breast cancer cells through regulating the expression and

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Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

Yinxu Zhang1, Xiaomei Liu, Teng Zuo

  • 1Department of General Surgery, The First Affiliated Hospital of Liaoning Medical University, 121001 Jinzhou, Liaoning, China. zhangyinxu@163.com

Medical Oncology (Northwood, London, England)
|May 13, 2011
PubMed

Insights

Tetramethylpyrazine (TMP) can overcome multidrug resistance (MDR) in breast cancer by increasing doxorubicin concentration and inhibiting P-glycoprotein (Pgp) activity and expression. This suggests TMP

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Tumor multidrug resistance (MDR) is a significant challenge in cancer chemotherapy.
  • The mechanisms by which compounds like tetramethylpyrazine (TMP) reverse MDR are not fully understood.

Purpose of the Study:

  • To investigate the effects of TMP on MDR in drug-resistant breast cancer cells.
  • To elucidate the underlying molecular mechanisms of TMP's action against MDR.

Main Methods:

  • Utilized MTT assays to assess cell growth inhibition.
  • Employed flow cytometry to evaluate doxorubicin accumulation.
  • Detected P-glycoprotein (Pgp) expression via Western blot and RT-PCR.

Main Results:

  • TMP dose-dependently increased intracellular doxorubicin concentration.
  • TMP inhibited Pgp-mediated doxorubicin efflux.
  • TMP suppressed Pgp ATPase activity and Pgp expression in MCF-7/dox cells.

Conclusions:

  • TMP demonstrates potential in reversing MDR in breast cancer.
  • TMP acts by inhibiting Pgp function and expression, enhancing chemotherapy efficacy.

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