Cucurbitacin B inhibits proliferation and induces apoptosis via STAT3 pathway inhibition in A549 lung cancer cells.

Abstract

Natural products are a great source of cancer chemotherapeutic agents. The present study was conducted to investigate whether cucurbitacin B (CuB), one of the most potent and widely used cucurbitacins, inhibits proliferation and induces apoptosis in the A549 lung cancer cell line. Furthermore, CuB induced apoptosis of A549 cells in a -concentration-dependent manner, as determined by fluorescence microscopy, flow cytometry and transmission electron microscopy. The present study also demonstrated that CuB dose-dependently inhibited lung cancer cell proliferation, with cell cycle inhibition and cyclin B1 downregulation. Apoptosis induced by CuB was shown to be associated with cytochrome c release, B-cell lymphoma 2 downregulation and signal transducer and activator of transcription 3 pathway inhibition. CuB may prove to be a useful approach for the chemotherapy of lung cancer.

• Authors: Meng Zhang, Zhi-Gang Bian, Yi Zhang, Jia-He Wang, Liang Kan, Xin Wang, Hui-Yan Niu, Ping He
• Journal: Molecular medicine reports (Mol Med Rep) Vol. 10 Issue 6 Pg. 2905-11 (Dec 2014) ISSN: 1791-3004 [Electronic] Greece
• PMID: 25242136 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antineoplastic Agents
• Cyclin B1
• Proto-Oncogene Proteins c-bcl-2
• STAT3 Transcription Factor
• STAT3 protein, human
• Triterpenes
• cucurbitacin B
• Cytochromes c

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Cell Cycle (drug effects)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Cyclin B1 (metabolism)
• Cytochromes c (metabolism)
• Down-Regulation (drug effects)
• Humans
• Lung Neoplasms (drug therapy)
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• STAT3 Transcription Factor (metabolism)
• Signal Transduction (drug effects)
• Triterpenes (pharmacology)