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Crude extract and solvent fractions of Calystegia soldanella induce G1 and S phase arrest of the cell cycle in HepG2 cells

  • Authors:
    • Jung Im Lee
    • In-Hye Kim
    • Taek-Jeong Nam
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    Affiliations: Institute of Fisheries Science, Pukyong National University, Ilgwang-myeon, Gijang-gun, Busan 619-911, Republic of Korea
    Copyright: © Lee et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 414-420
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    Published online on: January 2, 2017
       https://doi.org/10.3892/ijo.2017.3836
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Abstract

The representative halophyte Calystegia soldanella (L) Roem. et Schult is a perennial vine herb that grows in coastal dunes throughout South Korea as well as in other regions around the world. This plant has long been used as an edible and medicinal herb to cure rheumatic arthritis, sore throat, dropsy, and scurvy. Some studies have also shown that this plant species exhibits various biological activities. However, there are few studies on cytotoxicity induced by C. soldanella treatment in HepG2 human hepatocellular carcinoma cells. In this study, we investigated the viability of HepG2 cells following treatment with crude extracts and four solvent-partitioned fractions of C. soldanella. Of the crude extract and four solvent fractions tested, treatment with the 85% aqueous methanol (aq. MeOH) fraction resulted in the greatest inhibition of HepG2 cell proliferation. Flow cytometry showed that the 85% aq. MeOH fraction induced a G0/G1 and S phase arrest of the cell cycle progression. The 85% aq. MeOH fraction arrested HepG2 cells at the G0/G1 phase in a concentration-dependent manner, and resulted in decreased expression of cyclin D1, cyclin E, cyclin-dependent kinase (CDK)2, CDK4, CDK6, p21, and p27. Additionally, the 85% aq. MeOH fraction treatment also arrested HepG2 cells in the S phase, with decreased expression of cyclin A, CDK2, and CDC25A. Also, treatment with this fraction reduced the expression of retinoblastoma (RB) protein and the transcription factor E2F. These results suggest that the 85% aq. MeOH fraction exhibits potential anticancer activity in HepG2 cells by inducing G0/G1 and S phase arrest of the cell cycle.
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Copy and paste a formatted citation
Spandidos Publications style
Lee JI, Kim I and Nam T: Crude extract and solvent fractions of Calystegia soldanella induce G1 and S phase arrest of the cell cycle in HepG2 cells. Int J Oncol 50: 414-420, 2017.
APA
Lee, J.I., Kim, I., & Nam, T. (2017). Crude extract and solvent fractions of Calystegia soldanella induce G1 and S phase arrest of the cell cycle in HepG2 cells. International Journal of Oncology, 50, 414-420. https://doi.org/10.3892/ijo.2017.3836
MLA
Lee, J. I., Kim, I., Nam, T."Crude extract and solvent fractions of Calystegia soldanella induce G1 and S phase arrest of the cell cycle in HepG2 cells". International Journal of Oncology 50.2 (2017): 414-420.
Chicago
Lee, J. I., Kim, I., Nam, T."Crude extract and solvent fractions of Calystegia soldanella induce G1 and S phase arrest of the cell cycle in HepG2 cells". International Journal of Oncology 50, no. 2 (2017): 414-420. https://doi.org/10.3892/ijo.2017.3836
Copy and paste a formatted citation
x
Spandidos Publications style
Lee JI, Kim I and Nam T: Crude extract and solvent fractions of Calystegia soldanella induce G1 and S phase arrest of the cell cycle in HepG2 cells. Int J Oncol 50: 414-420, 2017.
APA
Lee, J.I., Kim, I., & Nam, T. (2017). Crude extract and solvent fractions of Calystegia soldanella induce G1 and S phase arrest of the cell cycle in HepG2 cells. International Journal of Oncology, 50, 414-420. https://doi.org/10.3892/ijo.2017.3836
MLA
Lee, J. I., Kim, I., Nam, T."Crude extract and solvent fractions of Calystegia soldanella induce G1 and S phase arrest of the cell cycle in HepG2 cells". International Journal of Oncology 50.2 (2017): 414-420.
Chicago
Lee, J. I., Kim, I., Nam, T."Crude extract and solvent fractions of Calystegia soldanella induce G1 and S phase arrest of the cell cycle in HepG2 cells". International Journal of Oncology 50, no. 2 (2017): 414-420. https://doi.org/10.3892/ijo.2017.3836
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