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Epieriocalyxin A Induces Cell Apoptosis Through JNK and ERK1/2 Signaling Pathways in Colon Cancer Cells

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Abstract

Colorectal cancer is one of the most commonly diagnosed cancers in the world. Currently, drug resistance of cancer cell to chemotherapy is a major cause for cancer recurrence and death of the patients; therefore, new therapeutic strategy is required to improve the care of colorectal cancer patients. The Chinese herb, Isodon eriocalyx, has been used a therapeutic for a long time in China. In this study, we showed that Epieriocalyxin A (EpiA), a diterpenoid isolated from I. eriocalyx, suppressed Caco-2 colon cancer cell growth. EpiA induced annexin V flipping in cell membrane and DNA fragment. We also showed that EpiA induced the generation of ROS in cells, as well as damage of the mitochondrial membrane. Western blot results showed that both JNK and ERK1/2 activation was decreased after EpiA treatment in a dose-dependent manner. EpiA increased the expression of caspase 3 and Bax, and decreased Bcl2 expression. Our results suggest that EpiA is a novel compound that induces colon cancer apoptosis. EpiA could be a potential drug for colon cancer therapy in the future.

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Authors and Affiliations

  1. Department of Hepatobiliary Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People’s Republic of China

    Zhou Wang, Zhengchuan Niu, Benjia Liang & Jun Niu

  2. Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Public Health, Jinan, 250012, Shandong, People’s Republic of China

    Zhou Wang, Zhengchuan Niu & Benjia Liang

  3. Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People’s Republic of China

    Zhijie Xu

Authors
  1. Zhou Wang
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  2. Zhijie Xu
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  3. Zhengchuan Niu
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  4. Benjia Liang
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  5. Jun Niu
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Correspondence to Jun Niu.

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Wang, Z., Xu, Z., Niu, Z. et al. Epieriocalyxin A Induces Cell Apoptosis Through JNK and ERK1/2 Signaling Pathways in Colon Cancer Cells. Cell Biochem Biophys 73, 559–564 (2015). https://doi.org/10.1007/s12013-015-0687-4

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  • DOI: https://doi.org/10.1007/s12013-015-0687-4

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