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Gallic acid targets acute myeloid leukemia via Akt/mTOR-dependent mitochondrial respiration inhibition

Ruixin Gu1, Minqin Zhang1, Hu Meng2

  • 1Department of Traditional Chinese Medicine, Wuhan Forth Hospital, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|June 9, 2018
PubMed

Insights

Gallic acid induces apoptosis in acute myeloid leukemia (AML) cells by inhibiting mitochondrial respiration through the Akt/mammalian target of rapamycin (mTOR) pathway. This natural compound enhances standard chemotherapy efficacy, offering a potential combination therapy for leukemia.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Gallic acid, a phenolic compound, exhibits anti-cancer properties, but its molecular mechanisms in acute myeloid leukemia (AML) remain unclear.
  • Understanding gallic acid's action is crucial for developing novel therapeutic strategies against AML.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying gallic acid's anti-leukemic effects in AML.
  • To investigate gallic acid's impact on mitochondrial respiration and its interaction with the Akt/mammalian target of rapamycin (mTOR) signaling pathway.
  • To evaluate gallic acid's potential as an adjunct therapy in AML treatment.

Main Methods:

  • Investigated gallic acid's effects on AML cell lines, primary mononuclear cells (MNC), and CD34 stem/progenitors.
  • Assessed apoptosis induction via caspase-dependent pathways.
  • Measured mitochondrial respiration, ATP production, and oxidative stress.
  • Utilized in vitro cell culture and in vivo xenograft models to evaluate combination therapy efficacy.
  • Examined the role of the Akt/mTOR signaling pathway using constitutively active Akt overexpression.

Main Results:

  • Gallic acid significantly induced apoptosis in AML cells and patient-derived samples through a caspase-dependent pathway.
  • Gallic acid inhibited mitochondrial respiration in a dose- and time-dependent manner, decreasing ATP production and increasing oxidative stress.
  • The Akt/mTOR signaling pathway was identified as a key mediator; Akt activation reversed gallic acid's effects on mTOR signaling, mitochondrial function, and apoptosis.
  • Gallic acid demonstrated synergistic effects with standard AML chemotherapeutic agents in both in vitro and in vivo models.

Conclusions:

  • Gallic acid exerts anti-leukemic effects in AML by suppressing mitochondrial respiration via the Akt/mTOR signaling pathway.
  • Gallic acid effectively induces apoptosis and enhances the efficacy of conventional chemotherapies in AML.
  • Combination therapy involving gallic acid holds promise for improving treatment outcomes in acute myeloid leukemia.
Keywords:
AMLAkt/mTORDrug combinationGallic acidMitochondrial respiration

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