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The role of Aurora‐A in curcumin‐enhanced chemosensitivity of human breast non‐metastatic cancer MCF‐7 and highly metastatic MDA‐MB‐231 cells
Author(s) -
Su ChunLi,
Yen ChengHsin,
Liu HsiaoSheng
Publication year - 2013
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.27.1_supplement.639.5
Subject(s) - curcumin , vinorelbine , cancer research , metastasis , kinase , apoptosis , pharmacology , cisplatin , cancer , metastatic breast cancer , medicine , cancer cell , chemistry , oncology , breast cancer , chemotherapy , biochemistry
Curcumin, an active compound in turmeric and curry, has been revealed to induce tumor apoptosis and inhibit tumor proliferation and metastasis. Overexpression of Aurora‐A, a mitosis‐related serine‐threonine kinase, increases drug resistance and promotes lung metastasis of breast cancer cells. Our previous results indicate that curcumin suppresses Aurora‐A kinase activity, induces S and G2/M mitotic arrest, and decreases proliferation of MCF‐7 and MDA‐MB‐231 cells. In the present study, combination therapy of curcumin with FDA‐approved anti‐cancer drugs (ixabepilone, cisplatin, vinorelbine, or everolimus) overrode chemoresistance in MDA‐MB‐231 cells. Addition of curcumin also enhanced cytotoxicity of ixabepilone in MCF‐7 cells. Induction of apoptosis and G2/M arrest, the consequences of Aurora‐A inhibition, were involved. However, addition of curcumin exhibited an antagonism effect in cisplatin, vinorelbine, or everolimus‐treated MCF‐7 cells due to not being able to suppress Aurora‐A kinase activity to a very low level. Therefore, the intake of diets rich in curcumin or curcumin‐containing supplements should be taken into consideration. (Supported in part by the National Science Council, Taiwan, No. NSC 98–2313‐B‐003–002‐MY3; the Ministry of Economic Affairs, Taiwan, No. 100‐EC‐17‐A‐17‐S1–152; and the National Taiwan Normal University, Taiwan, No. NTNU100‐D‐06).