Icariin induces cell differentiation and cell cycle arrest in mouse melanoma B16 cells via Erk1/2-p38-JNK-dependent pathway

Dan Wang, Wenjuan Xu, Xiaoyu Chen, Jichun Han, Lina Yu, Caixia Gao, Wenjin Hao, Xiaona Liu, Qiusheng Zheng, Defang LI*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

Abstract

Icariin (ICA) is a major component isolated from Epimedium brevicornum. Emerging evidence shows that ICA can inhibit tumor cell proliferation, invasion and migration. However, the anti-cancer effect of ICA on B16 cells has not been fully investigated. Here we found that the proliferation of B16 cells was inhibited by ICA in a concentration- and time-dependent manner, and the colony formation of B16 cells was also inhibited by ICA in a concentration-dependent manner. Further study showed that the melanin content was increased and the tyrosinase (Tyr) activity was enhanced after ICA treatment in B16 cells. Furthermore, compared with the control group, the mRNA levels of Tyr, Trp1 and Trp2 and the protein level of MITF were increased in ICA-treated B16 cells. In addition, the percentage of G0/G1 phase cells was increased and the protein levels of Cyclin A, CDK2 and p21 were decreased in ICAtreated B16 cells. Finally, we found that ICA increased down-regulated the Erk1/2, p-Erk1/2, p38, p-p38, and p-JNK protein levels in B16 cells when compared with the control group. Taken together, these results indicated that ICA could induce B16 cell differentiation and cell cycle arrest at G0/G1 phase through inhibiting Erk1/2-p38- JNK-dependent signaling molecules.

Original languageEnglish
Pages (from-to)99504-99513
Number of pages10
JournalOncotarget
Volume8
Issue number59
DOIs
Publication statusPublished - 2017

Scopus Subject Areas

  • Oncology

User-Defined Keywords

  • B16 cells
  • Cell-cycle arrest
  • Differentiation
  • Erk1/2-p38-JNK-dependent pathway
  • Icariin

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