Premium
3,4,2,4 Tetrahydroxychalcone (Butein) Inhibition of TNFα‐Induced CCL2 Release in Triple Negative Breast Cancer Cells
Author(s) -
Horton Anisley C,
Bauer David F.,
Soliman Karam F.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.809.1
Subject(s) - cancer research , chemokine , ccl2 , triple negative breast cancer , tumor necrosis factor alpha , breast cancer , tumor microenvironment , chemistry , monocyte , tumor progression , medicine , cancer , immunology , inflammation , tumor cells
Butein is a natural 3,4,2,4 tetrahydroxychalcone compound found in the Asian tree Rhus verniciflua, which is traditionally used for cancer treatment. Monocyte chemotactic protein‐1 (MCP‐1/CCL2) is released by tumor tissues, acting as a potent chemokine enabling the mononuclear cells to differentiate into tumor‐associated macrophages (TAMs). TAMs promote tumor progression, invasion, infiltration, and dissemination. The presence of TAMs in the tumors are associated with poor prognosis and increased mortality in breast cancers. Compounds, which can attenuate or inhibit the release of CCL2 have been shown to prevent cancer‐associated pro‐oncogenic processes. In this study; we evaluated the effects of butein on the release of TNFα ‐ induced tumor promoting chemokines in triple negative breast cancer (TNBC), MDA‐MB‐231 cells. Our studies were performed using antibody microarrays which specifically showed that TNFα (40 ng/mL) induced protein expression of CCL‐2, GM‐CSF, angiogenin, GRO‐alpha, osteoprotegerin and IL‐8, were attenuated by the administration of butein (5 μM). Moreover, the effects of butein on the attenuation of TNFα mediated CCL‐2 release were validated by ELISA (68% inhibition). These findings provide evidence to suggest that butein can modulate immunological signaling of cancer cells, which can prevent the cascades that direct TAMs infiltration, a pivotal role in tumor cell initiation, progression, invasion, and dissemination. Support or Funding Information Supported by NIH Grants G12 MD007582 and P20 MD 006738