Int J Med Sci 2019; 16(2):189-197. doi:10.7150/ijms.30647 This issue

Research Paper

Antarctic freshwater microalga, Chloromonas reticulata, suppresses inflammation and carcinogenesis

Sung-Suk Suh1*, Ju-Mi Hong2*, Eun Jae Kim2, Seung Won Jung3, Hyunsik Chae2, Jung Eun Kim2,4, Ji Hee Kim2,5, Il-Chan Kim2,5, Sanghee Kim2,5✉

1. Department of Bioscience, Mokpo National University, Muan 58554, Republic of Korea
2. Division of Polar Life Sciences, Korea Polar Research Institute, Incheon, 21990, Republic of Korea
3. South Sea Environment Research Department, Korea Institute of Ocean Science and Technology, Geoje, 656-830, Republic of Korea
4. Department of Pharmacy, Graduate School, Sungkyunkwan University, Suwan 16419, Republic of Korea
5. Department of Polar Sciences, University of Science and Technology, Incheon 21990, Republic of Korea
*These authors contributed equally to this study

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Suh SS, Hong JM, Kim EJ, Jung SW, Chae H, Kim JE, Kim JH, Kim IC, Kim S. Antarctic freshwater microalga, Chloromonas reticulata, suppresses inflammation and carcinogenesis. Int J Med Sci 2019; 16(2):189-197. doi:10.7150/ijms.30647. Available from

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Inflammation triggered by the innate immune system is a strategy to protect organisms from the risk of environmental infection. However, it has recently become clear that inflammation can cause a variety of human diseases, including cancer. In this study, we investigated the effects of an ethanol extract of the Antarctic freshwater microalgae, Chloromonas reticulata (ETCH), on inflammation and carcinogenesis in RAW 264.7 macrophages and HCT116 human colon cancer cells, respectively. ETCH exhibited significant anti-inflammatory activity through the dose-dependent modulation of major inflammatory markers such as COX-2, IL-6, iNOS, TNF-α, and NO production. For example, ETCH reduced LPS-induced upregulation of COX-2, IL-6, iNOS, and TNF- alpha mRNA levels, leading to a significant decrease in the levels of LPS-stimulated NO and IL-6 as well as TNF-alpha products. In contract, ETCH exhibited dose-dependent cytotoxic activity against HCT116 cells, yielding a profound reduction in the proliferation of the cancer cells. Furthermore, ETCH induced G2 phase cell cycle arrest by transcriptionally regulating of genes involved in G2 / M transition including p21 (CDKN1A), cyclin B1 (CCNB1), and CDK1; CDKN1A mRNA levels were upregulated in response to ETCH, whereas CCNB1 and CDK1 were downregulated. This study reports for the first time anti-inflammatory and anti-cancer effects of, C. reticulata and provides new insights into the molecular mechanisms of the linkage between inflammation and cancer.

Keywords: Inflammation cancer, Chloromonas reticulata, pro-inflammatory cytokines, HCT116