Blueberry phytochemicals inhibit growth and metastatic potential of MDA-MB-231 breast cancer cells through modulation of the phosphatidylinositol 3-kinase pathway
Adams LS, Phung S, Yee N, Seeram NP, Li L, Chen S
Cancer research · 128 citations
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- People, plus animal or lab work
- Main outcome
- Clinical events such as disease or death
Who paid for it
- Funding
- Independent funding
- Government
- National Institute of Environmental Health Sciences
- Government
- NIEHS NIH HHS
- Grants
- National Institute of Environmental Health Sciences (ES-08258); National Institute of Environmental Health Sciences (R01 ES008258)
Based on 2 listed funder(s).
Publication
- Published
- 2010-04-13 · Cancer Res · vol. 70 · issue 9 · pp. 3594–3605
- Publisher
- American Association for Cancer Research
- Cited
- 221 citations · more than 100% of similar papers · 14.6× the field average
- Impact
- Top 10% most cited in its field
- References
- 53 works
- Access
- Free to read
- Research areas
- Microbial Metabolism and Applications · Bioactive Compounds in Plants · Phytochemicals and Antioxidant Activities
- Keywords
- Protein kinase B, MAPK/ERK pathway, Cell growth, PI3K/AKT/mTOR pathway, Cancer research, Kinase, Chemistry, Biology, Signal transduction, Biochemistry
- MeSH
- cell line, tumor, animals, mice, inbred balb c, humans, mice, mice, nude, fruit, breast neoplasms, phenols, flavonoids, plasminogen activator inhibitor 1, tissue inhibitor of metalloproteinase-1, plant extracts, xenograft model antitumor assays, signal transduction, apoptosis, cell growth processes, cell movement, beverages, female, proto-oncogene proteins c-akt, matrix metalloproteinase 2, matrix metalloproteinase 9, urokinase-type plasminogen activator, phosphatidylinositol 3-kinases, polyphenols, matrix metalloproteinase inhibitors, blueberry plants
6 authors
From US
- Lynn S. AdamsUniversity of Rhode Island; City of Hope
- Sheryl PhungUniversity of Rhode Island; City of Hope
- Natalie YeeUniversity of Rhode Island; City of Hope
- Navindra Persaud SeeramUniversity of Rhode Island; City of Hope
- Liya LiUniversity of Rhode Island; City of Hope
- Shiuan Chen · correspondingUniversity of Rhode Island; City of Hope
Abstract
Dietary phytochemicals are known to exhibit a variety of anticarcinogenic properties. This study investigated the chemopreventive activity of blueberry extract in triple-negative breast cancer cell lines in vitro and in vivo. Blueberry decreased cell proliferation in HCC38, HCC1937, and MDA-MB-231 cells with no effect on the nontumorigenic MCF-10A cell line. Decreased metastatic potential of MDA-MB-231 cells by blueberry was shown through inhibition of cell motility using wound-healing assays and migration through a polyethylene terephthalate membrane. Blueberry treatment decreased the activity of matrix metalloproteinase-9 and the secretion of urokinase-type plasminogen activator while increasing tissue inhibitor of metalloproteinase-1 and plasminogen activator inhibitor-1 secretion in MDA-MB-231 conditioned medium as shown by Western blotting. Cell signaling pathways that control the expression/activation of these processes were investigated via Western blotting and reporter gene assay. Treatment with blueberry decreased phosphatidylinositol 3-kinase (PI3K)/AKT and NFkappaB activation in MDA-MB-231 cells, where protein kinase C and extracellular signal-regulated kinase (ERK) were not affected. In vivo, the efficacy of blueberry to inhibit triple-negative breast tumor growth was evaluated using the MDA-MB-231 xenograft model. Tumor weight and proliferation (Ki-67 expression) were decreased in blueberry-treated mice, where apoptosis (caspase-3 expression) was increased compared with controls. Immunohistochemical analysis of tumors from blueberry-fed mice showed decreased activation of AKT and p65 NFkappaB signaling proteins with no effect on the phosphorylation of ERK. These data illustrate the inhibitory effect of blueberry phytochemicals on the growth and metastatic potential of MDA-MB-231 cells through modulation of the PI3K/AKT/NFkappaB pathway.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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