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Apigenin as a Multitarget Anticancer Agent: Coordinated Inhibition of EGFR/MAPK and PI3K/Akt Signaling in Hematologic

Hatice Terzi1, Şeyma Taştemur2, Ayşegül Öztürk3

  • 1Department of Internal Medicine, Department of Hematology, Faculty of Medicine, Sivas Cumhuriyet University, 58140 Sivas, Türkiye.

International Journal of Molecular Sciences
|June 12, 2026
PubMed

Insights

Apigenin, a natural flavonoid, effectively reduced cancer cell viability in leukemia and lymphoma models. It suppressed key cancer growth pathways and induced apoptosis, showing promise for hematologic malignancies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Natural Products Chemistry

Background:

  • Hematologic malignancies involve aberrant growth and survival signaling pathways.
  • Dietary flavonoids like apigenin are explored for anticancer potential due to low toxicity.
  • Apigenin's specific molecular mechanisms in blood cancers are not well-defined.

Purpose of the Study:

  • To investigate the antineoplastic effects of apigenin in chronic myeloid leukemia (K562) and B-cell lymphoma (DOHH2) cell lines.
  • To elucidate the molecular pathways targeted by apigenin in these hematologic cancer models.
  • To assess the selectivity of apigenin using mouse fibroblast (L929) cells.

Main Methods:

  • Cell viability assessed via CCK-8 assay.
  • Signaling pathway analysis (EGFR, MAPK, PI3K, NF-κB) using ELISA.
  • Apoptosis and cell cycle distribution analyzed by flow cytometry.
  • Selectivity evaluated using L929 cells.

Main Results:

  • Apigenin demonstrated dose-dependent cytotoxicity with IC50 values of 84.14 μM (K562) and 70.11 μM (DOHH2).
  • Apigenin suppressed EGFR, MAPK, PI3K, and NF-κB signaling pathways and activated caspase-3 and caspase-7.
  • Apigenin induced S-phase cell cycle arrest and apoptosis, with minimal impact on L929 cells.

Conclusions:

  • Apigenin exhibits antiproliferative and pro-apoptotic effects in leukemia and lymphoma cells.
  • Inhibition of EGFR/MAPK and PI3K/Akt pathways and activation of caspase-mediated apoptosis underlie apigenin's action.
  • Apigenin's relative selectivity warrants further investigation in vivo and clinical trials for hematologic malignancies.
Keywords:
DOHH2K562apigeninapoptosisgrowth signaling pathwayshematological malignancies

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