Sulforaphane inhibits growth of phenotypically different breast cancer cells
Pawlik A, Wiczk A, Kaczyńska A, Antosiewicz J, Herman-Antosiewicz A
European journal of nutrition · 66 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
Based on full-text disclosure statement.
Publication
- Published
- 2013-02-06 · Eur J Nutr · vol. 52 · issue 8 · pp. 1949–1958
- Publisher
- Springer Science+Business Media
- Cited
- 89 citations · more than 93% of similar papers · 3.3× the field average
- Impact
- Top 10% most cited in its field
- References
- 51 works
- Access
- Open access (hybrid journal) · CC-BY
- Research areas
- Genomics, phytochemicals, and oxidative stress · PI3K/AKT/mTOR signaling in cancer · Synthesis and biological activity
- Keywords
- PI3K/AKT/mTOR pathway, Protein kinase B, P70-S6 Kinase 1, Cancer research, PTEN, Biology, Phosphorylation, Cell growth, Viability assay, Autophagy, Signal transduction, Chemistry, Cell biology, Cell, Apoptosis, Biochemistry
- MeSH
- cell line, tumor, humans, breast neoplasms, isothiocyanates, sulfoxides, ribosomal protein s6 kinases, 70-kda, microscopy, electron, transmission, signal transduction, cell proliferation, cell survival, phosphorylation, phenotype, autophagy, female, proto-oncogene proteins c-akt, pten phosphohydrolase, mcf-7 cells
5 authors
From PL
- Anna PawlikUniversity of Gdańsk
- Aleksandra WiczkUniversity of Gdańsk
- Angelika KaczyńskaUniversity of Gdańsk
- Jędrzej AntosiewiczGdańsk Medical University
- Anna Herman-Antosiewicz · correspondingUniversity of Gdańsk
Abstract
Purpose
Cancer development and resistance to chemotherapy correlates with aberrant activity of mitogenic pathways. In breast cancers, pro-survival PI3K-Akt-mTOR-S6K1 [corrected] signaling pathway is often hyperactive due to overexpression of genes coding for growth factors or estrogen receptors, constitutive activation of PI3K or Akt and loss of PTEN, a negative regulator of the pathway. Since epidemiologic as well as rodent tumor studies indicate that sulforaphane (SFN), a constituent of many edible cruciferous vegetables, might be a potent inhibitor of mammary carcinogenesis, we analyzed the response of four breast cancer cell lines representing different abnormalities in ErbB2/ER-PI3K-Akt-mTOR-S6K1[corrected] signaling pathway to this compound.
Methods
Four different breast cancer cell lines were used: MDA MB 231, MCF-7, SKBR-3 and MDA MB 468. Cell viability and ultrastructure, protein synthesis, autophagy induction and phosphorylation status of Akt and S6K1 kinases upon SFN treatment were determined.
Results
We observed that all four cell lines are similarly sensitive to SFN. SFN decreased phosphorylation of Akt and S6K1 kinases and at higher concentrations induced autophagy in all studied cell lines. Moreover, global protein synthesis was inhibited by SFN in investigated cell lines in a dose-dependent manner.
Conclusion
These results indicate that SFN is a potent inhibitor of the viability of breast cancer cells representing different activity of the ErbB2/ER-PI3K-Akt-mTOR-S6K1 [corrected] pro-survival pathway and suggest that it targets downstream elements of the pathway.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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