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Article

Arecoline suppresses HaCaT cell proliferation through cell cycle regulatory molecules

  • Authors:
    • Zhong-Su Zhou
    • Ming Li
    • Feng Gao
    • Jie-Ying Peng
    • Hai-Bo Xiao
    • Li-Xia Dai
    • Shi-Rong Lin
    • Rui Zhang
    • Long-Yu Jin
  • View Affiliations / Copyright

    Affiliations: Changsha Stomatological Hospital, Changsha, Hunan, P.R. China, The Third Xiangya Hospital of Central South University, Changsha, Hunan, P.R. China, Xiangya Hospital of Central South University, Changsha, Hunan, P.R. China, Taiwan Taipei Dental Sciences, Taipei, Taiwan, R.O.C.
  • Pages: 2438-2444
    |
    Published online on: March 22, 2013
       https://doi.org/10.3892/or.2013.2360
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Abstract

Betel nut chewing is the most common cause of oral submucous fibrosis (OSF). Arecoline is the main component of the betel nut, and is associated with the occurrence and development of OSF through cytotoxicity, genotoxicity and DNA damage. Similar types of stimuli elicit differential responses in different cells. In the present study, we investigated the effects of arecoline on the HaCaT epithelial and Hel fibroblast cell lines. The data showed that arecoline affected HaCaT cell morphology. MTT assay revealed that arecoline suppressed HaCaT cell proliferation. Furthermore, we found that arecoline induced the cell cycle arrest of HaCaT cells. In comparison with the untreated control cells, following treatment with ≥75 µg/ml arecoline an increased percentage of HaCaT cells remained at the G0/G1 phase of the cell cycle, accompanied by a reduced percentage of cells in the S phase. However, arecoline treatment did not significantly alter Hel cell cycle distribution. In the HaCaT epithelial cells, arecoline downregulated expression of the G1/S phase regulatory proteins cyclin D1, CDK4, CDK2, E2F1 as determined by reverse transcription-PCR analysis and western blotting. In summary, arecoline inhibits HaCaT epithelial cell proliferation and survival, in a dose-dependent manner, and cell cycle arrest in the G1/S phase, while this is not obvious in the Hel fibroblast cells. Potentially, our findings may aid in the prevention of arecoline-associated human OSF.
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Copy and paste a formatted citation
Spandidos Publications style
Zhou Z, Li M, Gao F, Peng J, Xiao H, Dai L, Lin S, Zhang R and Jin L: Arecoline suppresses HaCaT cell proliferation through cell cycle regulatory molecules. Oncol Rep 29: 2438-2444, 2013.
APA
Zhou, Z., Li, M., Gao, F., Peng, J., Xiao, H., Dai, L. ... Jin, L. (2013). Arecoline suppresses HaCaT cell proliferation through cell cycle regulatory molecules. Oncology Reports, 29, 2438-2444. https://doi.org/10.3892/or.2013.2360
MLA
Zhou, Z., Li, M., Gao, F., Peng, J., Xiao, H., Dai, L., Lin, S., Zhang, R., Jin, L."Arecoline suppresses HaCaT cell proliferation through cell cycle regulatory molecules". Oncology Reports 29.6 (2013): 2438-2444.
Chicago
Zhou, Z., Li, M., Gao, F., Peng, J., Xiao, H., Dai, L., Lin, S., Zhang, R., Jin, L."Arecoline suppresses HaCaT cell proliferation through cell cycle regulatory molecules". Oncology Reports 29, no. 6 (2013): 2438-2444. https://doi.org/10.3892/or.2013.2360
Copy and paste a formatted citation
x
Spandidos Publications style
Zhou Z, Li M, Gao F, Peng J, Xiao H, Dai L, Lin S, Zhang R and Jin L: Arecoline suppresses HaCaT cell proliferation through cell cycle regulatory molecules. Oncol Rep 29: 2438-2444, 2013.
APA
Zhou, Z., Li, M., Gao, F., Peng, J., Xiao, H., Dai, L. ... Jin, L. (2013). Arecoline suppresses HaCaT cell proliferation through cell cycle regulatory molecules. Oncology Reports, 29, 2438-2444. https://doi.org/10.3892/or.2013.2360
MLA
Zhou, Z., Li, M., Gao, F., Peng, J., Xiao, H., Dai, L., Lin, S., Zhang, R., Jin, L."Arecoline suppresses HaCaT cell proliferation through cell cycle regulatory molecules". Oncology Reports 29.6 (2013): 2438-2444.
Chicago
Zhou, Z., Li, M., Gao, F., Peng, J., Xiao, H., Dai, L., Lin, S., Zhang, R., Jin, L."Arecoline suppresses HaCaT cell proliferation through cell cycle regulatory molecules". Oncology Reports 29, no. 6 (2013): 2438-2444. https://doi.org/10.3892/or.2013.2360
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