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Although the antitumor activity of the crude extract of wild bitter gourd ( Momordica charantia  L.) has been reported, its bioactive constituents and the underlying mechanism remain undefined. Here, we report that 3  β  ,7  β  -dihydroxy-25-methoxycucurbita-5,23-diene-19-al (DMC), a cucurbitane-type triterpene isolated from wild bitter gourd, induced apoptotic death in breast cancer cells through peroxisome proliferator-activated receptor (PPAR)   γ   activation. Luciferase reporter assays indicated the ability of DMC to activate PPAR  γ  , and pharmacological inhibition of PPAR  γ   protected cells from DMC's antiproliferative effect. Western blot analysis indicated that DMC suppressed the expression of many PPAR  γ  -targeted signaling effectors, including cyclin D1, CDK6, Bcl-2, XIAP, cyclooxygenase-2, NF-  κ  B, and estrogen receptor   α  , and induced endoplasmic reticulum stress, as manifested by the induction of GADD153 and GRP78 expression. Moreover, DMC inhibited mTOR-p70S6K signaling through Akt downregulation and AMPK activation. The ability of DMC to activate AMPK in liver kinase (LK) B1-deficient MDA-MB-231 cells suggests that this activation was independent of LKB1-regulated cellular metabolic status. However, DMC induced a cytoprotective autophagy presumably through mTOR inhibition, which could be overcome by the cotreatment with the autophagy inhibitor chloroquine. Together, the ability of DMC to modulate multiple PPAR  γ  -targeted signaling pathways provides a mechanistic basis to account for the antitumor activity of wild bitter gourd.

evidence-based complementary and alternative medicine

Cucurbitane Triterpenoid from<i>Momordica charantia</i>Induces Apoptosis and Autophagy in Breast Cancer Cells, in Part, through Peroxisome Proliferator-Activated Receptor<i>γ</i>Activation

Cucurbitane Triterpenoid fromMomordica charantiaInduces Apoptosis and Autophagy in Breast Cancer Cells, in Part, through Peroxisome Proliferator-Activated ReceptorγActivation