The growth of a variety of tumors are inhibited by indole-3-carbinol (I3C) obviously. But, its role in laryngeal cancer is not clear. The goal of this study was to research the probable roles that laryngeal cancer cell apoptosis and proliferation Hep-2 was influenced by I3C. I3C dose-dependently therapy obviously inhibited Hep-2cell proliferation, and, I3C promoted apoptosis and induced cell morphological changes at 100, 200, 300, 400 μM doses. We discovered that I3C shows anticancer effect through various signal pathways after Hep-2 cells I3C therapy. In Hep-2laryngeal cancer cell line, through decreasing cell cycle-related proteins that include cyclin D1, CDK6, CDK4, and pRb, G1 arrest was induced by I3C. Apart from this, BALB/c nude mice constructed tumor-bearing mouse models. BALB/c nude mice were divided into three groups: treated with I3C, untreated control group and pretreated with I3C. After 8 weeks treatment, the untreated control group developed bigger tumors compared to mice treated or pretreated with I3C, and in the tumors such as cyclin D1, CDK6, CDK4 and pRb cell cycle-related proteins were obviously decreased. Further, the study result showed there was no harmful side effect in the heart, liver and kidney of the I3C-treated nude mice. In conclusion, both in vivo and in vitro I3C inhibited proliferation and induced the Hep-2 cells apoptosis, and showed low toxicity to normal cells. By suppressing the expression of cyclin families and CDK, we deduce that I3C can inhibit the Hep-2 cells growth in vitro. On normal organs and tissues, the I3C had no toxic effects and was safe.
| Published in | Journal of Diseases and Medicinal Plants (Volume 5, Issue 2) |
| DOI | 10.11648/j.jdmp.20190502.11 |
| Page(s) | 22-28 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2019. Published by Science Publishing Group |
Laryngeal Cancer, Indole-3-carbinol, Cell Cycle, Apoptosis
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APA Style
Chenggang Mao, Xiaochun Zhou, Yidao Jiang, Lijia Wan, Zezhang Tao. (2019). Indole-3-Carbinol Inhibits Laryngeal Cancer Growth Through Cell Cycle Arrest. Journal of Diseases and Medicinal Plants, 5(2), 22-28. https://doi.org/10.11648/j.jdmp.20190502.11
ACS Style
Chenggang Mao; Xiaochun Zhou; Yidao Jiang; Lijia Wan; Zezhang Tao. Indole-3-Carbinol Inhibits Laryngeal Cancer Growth Through Cell Cycle Arrest. J. Dis. Med. Plants 2019, 5(2), 22-28. doi: 10.11648/j.jdmp.20190502.11
AMA Style
Chenggang Mao, Xiaochun Zhou, Yidao Jiang, Lijia Wan, Zezhang Tao. Indole-3-Carbinol Inhibits Laryngeal Cancer Growth Through Cell Cycle Arrest. J Dis Med Plants. 2019;5(2):22-28. doi: 10.11648/j.jdmp.20190502.11
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Download@article{10.11648/j.jdmp.20190502.11,
author = {Chenggang Mao and Xiaochun Zhou and Yidao Jiang and Lijia Wan and Zezhang Tao},
title = {Indole-3-Carbinol Inhibits Laryngeal Cancer Growth Through Cell Cycle Arrest},
journal = {Journal of Diseases and Medicinal Plants},
volume = {5},
number = {2},
pages = {22-28},
doi = {10.11648/j.jdmp.20190502.11},
url = {https://doi.org/10.11648/j.jdmp.20190502.11},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.jdmp.20190502.11},
abstract = {The growth of a variety of tumors are inhibited by indole-3-carbinol (I3C) obviously. But, its role in laryngeal cancer is not clear. The goal of this study was to research the probable roles that laryngeal cancer cell apoptosis and proliferation Hep-2 was influenced by I3C. I3C dose-dependently therapy obviously inhibited Hep-2cell proliferation, and, I3C promoted apoptosis and induced cell morphological changes at 100, 200, 300, 400 μM doses. We discovered that I3C shows anticancer effect through various signal pathways after Hep-2 cells I3C therapy. In Hep-2laryngeal cancer cell line, through decreasing cell cycle-related proteins that include cyclin D1, CDK6, CDK4, and pRb, G1 arrest was induced by I3C. Apart from this, BALB/c nude mice constructed tumor-bearing mouse models. BALB/c nude mice were divided into three groups: treated with I3C, untreated control group and pretreated with I3C. After 8 weeks treatment, the untreated control group developed bigger tumors compared to mice treated or pretreated with I3C, and in the tumors such as cyclin D1, CDK6, CDK4 and pRb cell cycle-related proteins were obviously decreased. Further, the study result showed there was no harmful side effect in the heart, liver and kidney of the I3C-treated nude mice. In conclusion, both in vivo and in vitro I3C inhibited proliferation and induced the Hep-2 cells apoptosis, and showed low toxicity to normal cells. By suppressing the expression of cyclin families and CDK, we deduce that I3C can inhibit the Hep-2 cells growth in vitro. On normal organs and tissues, the I3C had no toxic effects and was safe.},
year = {2019}
}
TY - JOUR T1 - Indole-3-Carbinol Inhibits Laryngeal Cancer Growth Through Cell Cycle Arrest AU - Chenggang Mao AU - Xiaochun Zhou AU - Yidao Jiang AU - Lijia Wan AU - Zezhang Tao Y1 - 2019/06/04 PY - 2019 N1 - https://doi.org/10.11648/j.jdmp.20190502.11 DO - 10.11648/j.jdmp.20190502.11 T2 - Journal of Diseases and Medicinal Plants JF - Journal of Diseases and Medicinal Plants JO - Journal of Diseases and Medicinal Plants SP - 22 EP - 28 PB - Science Publishing Group SN - 2469-8210 UR - https://doi.org/10.11648/j.jdmp.20190502.11 AB - The growth of a variety of tumors are inhibited by indole-3-carbinol (I3C) obviously. But, its role in laryngeal cancer is not clear. The goal of this study was to research the probable roles that laryngeal cancer cell apoptosis and proliferation Hep-2 was influenced by I3C. I3C dose-dependently therapy obviously inhibited Hep-2cell proliferation, and, I3C promoted apoptosis and induced cell morphological changes at 100, 200, 300, 400 μM doses. We discovered that I3C shows anticancer effect through various signal pathways after Hep-2 cells I3C therapy. In Hep-2laryngeal cancer cell line, through decreasing cell cycle-related proteins that include cyclin D1, CDK6, CDK4, and pRb, G1 arrest was induced by I3C. Apart from this, BALB/c nude mice constructed tumor-bearing mouse models. BALB/c nude mice were divided into three groups: treated with I3C, untreated control group and pretreated with I3C. After 8 weeks treatment, the untreated control group developed bigger tumors compared to mice treated or pretreated with I3C, and in the tumors such as cyclin D1, CDK6, CDK4 and pRb cell cycle-related proteins were obviously decreased. Further, the study result showed there was no harmful side effect in the heart, liver and kidney of the I3C-treated nude mice. In conclusion, both in vivo and in vitro I3C inhibited proliferation and induced the Hep-2 cells apoptosis, and showed low toxicity to normal cells. By suppressing the expression of cyclin families and CDK, we deduce that I3C can inhibit the Hep-2 cells growth in vitro. On normal organs and tissues, the I3C had no toxic effects and was safe. VL - 5 IS - 2 ER -
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