12-Chloracetyl-PPD, A Novel Dammarane Derivative, Shows Anti-Cancer Activity by Delaying G2/M Phase Cell Cycle Progression and Inducing ROS-Mediated Apoptosis

    Xu De Wang, Yuan Sun, Chen Zhao, Fan Qu, Yu Zhao
    TLDR A new compound slows cancer cell growth and causes cell death by blocking cell cycle progression and increasing cell-damaging molecules.
    The study investigated the anti-cancer mechanisms of 12-Chloracetyl-PPD, a modified ginsenoside derived from Panax ginseng. The compound showed concentration-dependent inhibition of viability in prostate, breast, and gastric cancer cells, while sparing normal cells such as human gastric epithelial cells, hair follicle dermal papilla cells, and rat myocardial cells. In MDA-MB-435 and C4-2B cancer cells, 12-Chloracetyl-PPD induced G2/M cell cycle arrest, down-regulated MDM2 expression, up-regulated p53 expression, triggered apoptosis, and increased reactive oxygen species production. The apoptosis effect was mitigated by the reactive oxygen species scavenger N-acetylcysteine. These findings suggested that 12-Chloracetyl-PPD could be a potential agent for cancer chemotherapy by delaying cell cycle progression and inducing apoptosis through reactive oxygen species production.
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