Tier 3 — preclinical

Pharmacological Properties of 4′, 5, 7-Trihydroxyflavone (Apigenin) and Its Impact on Cell Signaling Pathways

Rameesha Abid, Shakira Ghazanfar, Arshad Farid, Samra Muhammad Sulaman, Maryam Idrees, Radwa Abdallnasser Amen, Muhammad Muzammal, Muhammad Khurram Shahzad, Mohamed Omar Mohamed, Alaa Ashraf Khaled, Waqas Safir, Ifra Ghori, Abdelbaset Mohamed Elasbali, Bandar Alharbi
Molecules 2022 27(13):4304

Bibliography

PubMed
PMID 35807549
PubMed Central
PMC9267958
Funding
The review reports research support including grant DSR-2021-01-0369.
Competing interests
The authors declared no conflict of interest.

Study snapshot

DesignNarrative pharmacology and cell-signaling review
ModelPublished in vitro, animal and limited clinical-context literature
SampleNot applicable; review article.
InterventionApigenin across published models, with emphasis on PI3K/AKT/mTOR, JAK/STAT, NF-kB and ERK/MAPK signaling.
DurationNot applicable.
EndpointsPI3K/AKT/mTOR signaling; JAK/STAT signaling; NF-kB signaling; ERK/MAPK signaling; Apoptosis; Autophagy; Cell proliferation and migration

What the study showed, in plain terms

This review organizes the many signaling pathways reported to respond to apigenin, especially in cancer models. It is useful for understanding proposed mechanisms, but most of the cited effects come from cells or animals rather than controlled human apigenin trials.

Key findings

Recurring mechanistic themes include suppression of PI3K/AKT/mTOR and NF-kB signaling, modulation of JAK/STAT and ERK/MAPK pathways, promotion of apoptosis and autophagy, and reduced proliferation or migration in numerous cancer-cell models.

What this study can and cannot tell us

The review synthesizes heterogeneous experimental models and does not provide pooled clinical effect estimates. Mechanistic activity at experimental concentrations should not be treated as evidence that oral apigenin prevents or treats cancer in humans.

Editorial review

Reviewed by the Biohack Blueprint research team

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