Abstract Title:

Emodin promotes the arrest of human lymphoma Raji cell proliferation through the UHRF1‑DNMT3A‑∆Np73 pathways.

Abstract Source:

Mol Med Rep. 2017 Nov ;16(5):6544-6551. Epub 2017 Sep 5. PMID: 28901428

Abstract Author(s):

Yun Lin, Weiming Chen, Zhihong Wang, Pengwei Cai

Article Affiliation:

Yun Lin


Emodin is an active constituent found in the roots and rhizomes of numerous Chinese medicinal herbs. It exerts antitumor activity against Dalton's lymphoma in vivo, although the detailed mechanisms by which emodin induces apoptosis remains to be elucidated. The present study aimed to analyze the mechanisms underlying the response to emodin treatment. Using lymphoma Raji cells, an emodin‑induced cell proliferating inhibition model was first established, then flow cytometry, western blotting, reverse transcription‑quantitative polymerase chain reaction and luciferase reporter assay were performed. It was found that emodin decreased the percentage of Raji cell viability, induced apoptosis, and increased the activation of caspase 3, caspase 9 andpoly (ADP‑ribose) polymerase through the downregulation of ubiquitin‑like protein containing PHD and RING domains 1 (UHRF1). The emodin‑induced downregulation of UHRF1 led to an increase in the level of DNA methyltransferase 3A, which in turn inhibited the activity of p73 promoter 2 and decreased the levels of NH2‑terminally truncated dominant‑negative p73. The treatment of Raji cells with emodin combined with doxorubicin led increased cell death of Raji cells, indicating that emodin may sensitize Raji cells to doxorubicin‑induced apoptosis.

Study Type : In Vitro Study

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