# From Phytochemistry to Oncology: The Role of Bakuchiol in the Treatment of Breast Cancer

**Authors:** Magdalena Czarnecka-Czapczyńska, David Aebisher, Alina Pietryszyn-Bilińska, Magdalena Moś, Sara Czech, Jakub Szpara, Dorota Bartusik-Aebisher, Aleksandra Kawczyk-Krupka

PMC · DOI: 10.3390/biom16010094 · Biomolecules · 2026-01-06

## TL;DR

This review explores how bakuchiol, a natural compound, may help treat breast cancer by affecting multiple biological pathways.

## Contribution

The paper systematically reviews the molecular mechanisms and therapeutic potential of bakuchiol in breast cancer.

## Key findings

- Bakuchiol modulates oxidative stress, apoptosis, and key signaling pathways in breast cancer cells.
- It suppresses cancer stem-cell renewal and reduces metastasis drivers in breast cancer models.
- Bakuchiol's effects are particularly notable in estrogen receptor-positive breast cancer cells.

## Abstract

Bakuchiol (BAK), a natural meroterpenoid with antioxidant, anti-inflammatory and anticancer properties, has recently gained attention as a potential adjunct in breast cancer therapy. This review contextualizes breast cancer as a major global health challenge and highlights BAK as a bioactive compound capable of modulating pathways relevant to tumor development and progression. A structured literature search identified studies examining its molecular activity, pharmacological profile, and effects on breast cancer cells and stem cells. Results show that BAK influences oxidative stress regulation, mitochondrial function, apoptosis and estrogen receptor signaling while also affecting PI3K/AKT, MAPK, NF-κB, and EMT-related pathways. In breast cancer models, BAK acts as a selective phytoestrogen, induces S-phase arrest, activates the ATM/ATR–Chk1/Chk2 axis, and triggers mitochondrial apoptosis, particularly in ERα-positive cells. It also suppresses breast cancer stem-cell renewal, promotes BNIP3- and DAPK2-mediated apoptosis, reduces metabolic and transcriptional drivers of metastasis, and shows enhanced anticancer activity in derivative forms. These findings suggest that BAK may provide therapeutic benefit across several mechanisms central to breast cancer biology. In this review, the inclusion criteria encompassed publications describing the action of bakuchiol, its chemical and pharmacological properties, as well as its role in the treatment of various conditions, including cancers. Exclusion criteria included works not related to BAK or its therapeutic use in breast cancer, as well as publications that did not meet basic scientific standards, such as lacking methodological rigor or presenting a low level of scientific evidence. However, current evidence is predominantly in vitro, and limitations such as poor bioavailability and lack of clinical validation underscore the need for further in vivo and translational studies before therapeutic application can be established.

## Linked entities

- **Genes:** ESR1 (estrogen receptor 1) [NCBI Gene 2099], BNIP3 (BCL2 interacting protein 3) [NCBI Gene 664], DAPK2 (death associated protein kinase 2) [NCBI Gene 23604], PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) [NCBI Gene 5290], AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207], MAPK (mitogen activated kinase-like protein) [NCBI Gene 7446652], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790], ATM (ATM serine/threonine kinase) [NCBI Gene 472], ATR (ATR checkpoint kinase) [NCBI Gene 545], CHEK1 (checkpoint kinase 1) [NCBI Gene 1111], CHEK2 (checkpoint kinase 2) [NCBI Gene 11200]
- **Chemicals:** Bakuchiol (PubChem CID 5468522)
- **Diseases:** Breast cancer (MONDO:0004989)

## Full-text entities

- **Genes:** CHEK1 (checkpoint kinase 1) [NCBI Gene 1111] {aka CHK1, OZEMA21}, ATM (ATM serine/threonine kinase) [NCBI Gene 472] {aka AT1, ATA, ATC, ATD, ATDC, ATE}, DAPK2 (death associated protein kinase 2) [NCBI Gene 23604] {aka DRP-1, DRP1}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, ESR1 (estrogen receptor 1) [NCBI Gene 2099] {aka ER, ESR, ESRA, ESTRR, Era, NR3A1}, ATR (ATR checkpoint kinase) [NCBI Gene 545] {aka FCTCS, FRP1, MEC1, SCKL, SCKL1}, CHEK2 (checkpoint kinase 2) [NCBI Gene 11200] {aka CDS1, CHK2, HuCds1, LFS2, PP1425, RAD53}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, BNIP3 (BCL2 interacting protein 3) [NCBI Gene 664] {aka HABON, NIP3}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}
- **Diseases:** metastasis (MESH:D009362), inflammatory (MESH:D007249), Breast Cancer (MESH:D001943), cancers (MESH:D009369)
- **Chemicals:** BAK (MESH:C012765), meroterpenoid (-)

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12838981/full.md

## References

72 references — full list in the complete paper: https://tomesphere.com/paper/PMC12838981/full.md

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Source: https://tomesphere.com/paper/PMC12838981