Tier 3 — preclinical

Targeting the PI3K/Akt/mTOR axis by apigenin for cancer prevention

Xin Tong, Jill Pelling
Anti-Cancer Agents in Medicinal Chemistry 2013 13(7):971-978

Bibliography

PubMed
PMID 23272913
PubMed Central
PMC3729595
Funding
Specific funding was not identified in the uploaded manuscript text.
Competing interests
A competing-interests statement was not identified in the uploaded manuscript text.

Study snapshot

DesignNarrative mechanistic review
ModelPublished cancer-cell, keratinocyte and animal-model literature
SampleNot applicable; review article.
InterventionApigenin across experimental cancer and chemoprevention models.
DurationNot applicable.
EndpointsPI3K/Akt signaling; mTORC1/mTORC2 signaling; AMPK activation; Apoptosis; Autophagy; Angiogenesis; Cell-cycle regulation

What the study showed, in plain terms

This review explains how apigenin interacts with the PI3K/Akt/mTOR network in experimental cancer models. The pathway is biologically important for cell growth, survival and metabolism, but the review is mechanistic evidence rather than proof that oral apigenin prevents cancer in people.

Key findings

The literature reviewed suggests apigenin can suppress PI3K/Akt activity, activate AMPK through CaMKKbeta in keratinocytes and thereby restrain mTOR signaling. These changes are linked experimentally to apoptosis, autophagy, reduced angiogenic signaling and slower tumor-cell growth.

What this study can and cannot tell us

The article is a narrative review of heterogeneous preclinical studies. Concentrations and routes vary widely, and mechanistic activity in cells or tumors cannot establish clinical cancer prevention, treatment efficacy or a human dose.

Editorial review

Reviewed by the Biohack Blueprint research team

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