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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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Melatonin Overcomes Cancer Multidrug Resistance by Downregulating ABCB1 Expression and Modulating Mitochondrial

Alba López-Rodríguez1,2,3, Laura Martinez-Ruiz1,2,3, Raquel Morales-Gallel4,5

  • 1Institute of Biotechnology, Biomedical Research Center, Health Sciences Technology Park, University of Granada, Granada, Spain.

Journal of Pineal Research
|November 5, 2025
PubMed
Summary
This summary is machine-generated.

Melatonin combats multidrug resistance (MDR) in cancer by boosting mitochondrial reactive oxygen species (ROS), which limits ATP for efflux pumps. This enhances chemosensitivity in ABCB1-overexpressing cells and reduces tumor growth.

Keywords:
P‐glycoproteinapoptosishead and neck cancermelatoninmitochondriamultidrug resistancereactive oxygen species

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Area of Science:

  • Oncology
  • Biochemistry
  • Mitochondrial Biology

Background:

  • Multidrug resistance (MDR) is a significant obstacle in cancer chemotherapy.
  • Overexpression of ATP-binding cassette (ABC) transporters, like ABCB1, is a key driver of MDR.
  • Novel strategies are crucial to overcome resistance mediated by ABC transporters.

Purpose of the Study:

  • To investigate the mechanisms by which melatonin overcomes ABCB1-mediated MDR in cancer cells.
  • To elucidate the role of mitochondrial function in melatonin's MDR-reversing effects.
  • To evaluate melatonin's potential as an adjuvant therapy against chemoresistance.

Main Methods:

  • Assessed melatonin's effects on head and neck squamous cell carcinoma (CAL 27, SCC-9) and breast cancer (MCF-7) cell lines overexpressing ABCB1.
  • Analyzed melatonin's impact on mitochondrial function, reactive oxygen species (ROS) production, and ABCB1 expression.
  • Evaluated melatonin's efficacy in a CAL 27 xenograft mouse model.

Main Results:

  • Melatonin treatment induced mitochondrial ROS production, weakening chemoresistance.
  • ROS generation led to NADH oxidation to NAD+, limiting ATP availability for efflux pumps.
  • Melatonin decreased mitochondrial localization near the nucleus, downregulated ABCB1 expression, and reduced tumor volume in vivo.

Conclusions:

  • Melatonin enhances chemosensitivity in ABCB1-overexpressing cancer cells by modulating mitochondrial metabolism and redox balance.
  • Melatonin's ability to downregulate ABCB1 expression contributes to overcoming MDR.
  • Melatonin shows promise as an adjuvant therapy to combat multidrug resistance in cancer treatment.