Artesunate activates the ATF4-CHOP-CHAC1 pathway and affects ferroptosis in Burkitt's Lymphoma

Ning Wang, Guang Zhi Zeng, Jun Lin Yin*, Zhaoxiang Bian

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

139 Citations (Scopus)


Currently, there is no effective treatment for Burkitt's lymphoma in patients aged above 60 years, and thus research on effective treatment options for Burkitt's lymphoma has been gaining increasing attention. Artesunate has been identified as a novel effective growth suppressor in Burkitt's lymphoma. Here, we utilized molecular biology, transcriptome analysis, and other techniques to study artesunate-induced death of the Burkitt's lymphoma cells DAUDI and CA-46, the effect of artesunate on gene expression in DAUDI and CA-46 cells, and the effect of artesunate-induced ATF4-CHOP-CHAC1 pathway on ferroptosis. We also studied the inhibitory effects and ferroptosis induction of artesunate on CA-46 cells in mouse xenografts. Results showed that artesunate induced ferroptosis in DAUDI and CA-46 cells, as evidenced by the protective effect of liproxstatin-1, ferrostatin-1, and desferoxamine, resulting in an endoplasmic reticulum stress response, activation of the ATF4-CHOP-CHAC1 pathway enhanced ferroptosis in DAUDI and CA-46 cells. A mouse-transplanted tumor model showed that artesunate can inhibit the proliferation and induce ferroptosis of CA-46 cells in vivo. This study provides a novel perspective for the development of drugs against different types of Burkitt's lymphomas.

Original languageEnglish
Pages (from-to)533-539
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - 12 Nov 2019

Scopus Subject Areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

User-Defined Keywords

  • Artesunate
  • Burkitt's lymphoma
  • CHAC1
  • Ferroptosis
  • Xenograft


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