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Curcumin Inhibits DLD‐1 Colorectal Cancer Cell Proliferation by Modulating MicroRNA and Tumor Suppressor Gene Expression
Author(s) -
Adeyeni Temitope,
Vattathara Kenn,
Duggirala Rajat,
Selvamani Vijayalingam,
Ezekiel Uthayashanker
Publication year - 2015
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.29.1_supplement.721.8
Subject(s) - curcumin , microrna , epigenetics , cancer research , carcinogenesis , cancer cell , cell growth , cancer , chemistry , methylation , biology , pharmacology , gene , biochemistry , genetics
Phytochemicals are plant‐based, non‐toxic compounds that produce health benefits. Curcumin, a major phytochemical in turmeric, inhibits the proliferation of many types of cancer cells, both in vitro and in vivo. Phytochemicals subvert carcinogenesis by modifying methylation patterns normally maintained by cancer cells. This methylation modification mechanism indirectly influences the regulatory microRNA that maintains normal cell division. Earlier, we identified that curcumin exerts an antiproliferative effect on DLD‐1 colon cancer cells in a dose dependent manner. After 48‐hour treatment of DLD‐1 cells with curcumin, expression level of tumor suppressor gene, RASSF1A, and microRNA‐15a (miR‐15a) was evaluated. Normally, expression levels of both RASSF1A and miR‐15a were suppressed in DLD‐1 cells; however, upon curcumin treatment, expression levels of RASSF1A and miR‐15a were higher than those in vehicle‐treated controls. Also, the miR‐15a target, BMI1, was suppressed in curcumin‐treated cells. In summary, curcumin exerted an antiproliferative effect against colon cancer cells, possibly by an epigenetic mechanism. KV and RD were supported by the DeNardo Foundation Fellowship.