Furanodiene induces extrinsic and intrinsic apoptosis in doxorubicin-resistant MCF-7 breast cancer cells via NF-κB-independent mechanism

Zhang Feng Zhong, Hai Bing Yu, Chun Ming Wang, Wen An Qiang, Sheng Peng Wang, Jin Ming Zhang, Hua Yu, Liao Cui, Tie Wu, De Qiang Li, Yi Tao Wang*

*Corresponding author for this work

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

Chemotherapy is used as a primary approach in cancer treatment after routine surgery. However, chemo-resistance tends to occur when chemotherapy is used clinically, resulting in poor prognosis and recurrence. Currently, Chinese medicine may provide insight into the design of new therapies to overcome chemo-resistance. Furanodiene, as a heat-sensitive sesquiterpene, is isolated from the essential oil of Rhizoma Curcumae. Even though mounting evidence claiming that furanodiene possesses anti-cancer activities in various types of cancers, the underlying mechanisms against chemo-resistant cancer are not fully clear. Our study found that furanodiene could display anti-cancer effects by inhibiting cell viability, inducing cell cytotoxicity, and suppressing cell proliferation in doxorubicin-resistant MCF-7 breast cancer cells. Furthermore, furanodiene preferentially causes apoptosis by interfering with intrinsic/extrinsic-dependent and NF-?B-independent pathways in doxorubicin-resistant MCF-7 cells. These observations also prompt that furanodiene may be developed as a promising natural product for multidrug-resistant cancer therapy in the future.

Original languageEnglish (US)
Article number648
JournalFrontiers in Pharmacology
Volume8
Issue numberSEP
DOIs
StatePublished - Sep 14 2017

Keywords

  • Breast cancer
  • Cell apoptosis
  • Furanodiene
  • Intrinsic/extrinsic apoptosis
  • Multidrug resistance
  • NF-κB

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

Fingerprint Dive into the research topics of 'Furanodiene induces extrinsic and intrinsic apoptosis in doxorubicin-resistant MCF-7 breast cancer cells via NF-κB-independent mechanism'. Together they form a unique fingerprint.

  • Cite this