Growth inhibitory effect of Cucurbitacin E on breast cancer cells

Int J Clin Exp Pathol. 2013 Aug 15;6(9):1799-805. eCollection 2013.


Objective: Due its inhibitory effects on chemical carcinogenesis and inflammation, Cucurbitacins have been proposed as an effective agent for the prevention or treatment of human cancers. In this study, we aimed to explore the effect of Cucurbitacin E (CuE) on human breast cancer cells.

Methods: The inhibitory effect of CuE on proliferation of Bcap37 and MDA-MB-231 cells was assessed by MTT assay. The cell cycle distribution and cell apoptosis were determined by flow cytometry (FCM). The expression of pro-caspase 3, cleaved caspase 3, p21, p27 and the phosphorylation of signaling proteins was detected by Western Blotting.

Results: CuE inhibited the growth of human breast cancer cells in a dose and time-dependent manner. FCM analysis showed that CuE induced G2/M phase arrest and cell apoptosis. CuE treatment promoted the cleavage of caspase 3 and upregulated p21 and p27. In addition, the phosphorylation of STAT3 but not ERK-1/2 was abrogated upon CuE treatment. Interestingly, losedose CuE significantly enhanced the growth inhibition induced by cisplatin. Conclusions Cucurbitacin E (CuE) could inhibit the growth of human breast cancer cells in vitro. CuE induced both apoptosis and cell cycle arrest probably through the inhibition of STAT3 function. Lose-dose CuE significantly enhanced the growth inhibitory effect of cisplatin on breast cancer cells, further indicating the potential clinical values of CuE for the prevention or treatment of human breast cancer.

Keywords: Cucurbitacin E; apoptosis; breast cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology
  • Apoptosis / drug effects
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology*
  • Caspase 3 / metabolism
  • Cell Cycle Checkpoints / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Cisplatin / pharmacology
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Cyclin-Dependent Kinase Inhibitor p27 / metabolism
  • Dose-Response Relationship, Drug
  • Drug Synergism
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Female
  • Humans
  • Phosphorylation
  • Prohibitins
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction / drug effects
  • Time Factors
  • Triterpenes / pharmacology*


  • Antineoplastic Agents, Phytogenic
  • CDKN1A protein, human
  • CDKN1B protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • PHB2 protein, human
  • Prohibitins
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Triterpenes
  • Cyclin-Dependent Kinase Inhibitor p27
  • Extracellular Signal-Regulated MAP Kinases
  • CASP3 protein, human
  • Caspase 3
  • Cisplatin
  • cucurbitacin E