Cucurbitacin E induces cell cycle G2/M phase arrest and apoptosis in triple negative breast cancer

Yanjie Kong; Jianchao Chen; Zhongmei Zhou; Houjun Xia; Ming-Hua Qiu; Ceshi Chen

doi:10.1371/journal.pone.0103760

Cucurbitacin E induces cell cycle G2/M phase arrest and apoptosis in triple negative breast cancer

PLoS One. 2014 Jul 29;9(7):e103760. doi: 10.1371/journal.pone.0103760. eCollection 2014.

Authors

Yanjie Kong¹, Jianchao Chen², Zhongmei Zhou³, Houjun Xia³, Ming-Hua Qiu², Ceshi Chen³

Affiliations

¹ Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China; Kunming College of Life Science, University of Chinese Academy of Sciences, Kunming, Yunnan, China.
² State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany, Chinese Academy of Science, Kunming, Yunnan, China.
³ Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China.

Abstract

Triple negative breast cancer (TNBC) is a highly aggressive form of breast cancer resistant to many common treatments. In this study, we compared the effects of 12 phytochemical drugs on four cancer cell lines, and noticed that Cucurbitacin E (CuE) significantly inhibited TNBC cell growth by inducing cell cycle G2/M phase arrest and apoptosis. CuE reduced expression of Cyclin D1, Survivin, XIAP, Bcl2, and Mcl-1 in MDA-MB-468 and SW527, and within MDA-MB-468, CuE significantly increased activation of JNK and inhibited activation of AKT and ERK. Collectively, these results suggest that CuE may be a viable compound for developing novel TNBC therapeutics.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Antineoplastic Agents, Phytogenic / chemistry
Antineoplastic Agents, Phytogenic / isolation & purification
Antineoplastic Agents, Phytogenic / pharmacology*
Apoptosis / drug effects*
Apoptosis Regulatory Proteins / metabolism
Cell Line, Tumor
Cyclins / metabolism
Extracellular Signal-Regulated MAP Kinases / metabolism
Female
G2 Phase Cell Cycle Checkpoints / drug effects*
Humans
JNK Mitogen-Activated Protein Kinases / metabolism
M Phase Cell Cycle Checkpoints / drug effects*
Orchidaceae / chemistry
Orchidaceae / metabolism
Plant Extracts / chemistry
STAT3 Transcription Factor / metabolism
Triple Negative Breast Neoplasms / metabolism
Triple Negative Breast Neoplasms / pathology
Triterpenes / chemistry
Triterpenes / isolation & purification
Triterpenes / pharmacology*

Substances

Antineoplastic Agents, Phytogenic
Apoptosis Regulatory Proteins
Cyclins
Plant Extracts
STAT3 Transcription Factor
Triterpenes
Extracellular Signal-Regulated MAP Kinases
JNK Mitogen-Activated Protein Kinases
cucurbitacin E

Grants and funding

This work was supported by National Natural Science Foundation of China (81120108019, U1132605, and 81325016 to Chen, C; U1192604 and 39970086 to Qiu, M). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.