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Allicin-Mediated Cell Cycle Regulation Reverses Taxol Resistance in NSCLC: Molecular Insights and Therapeutic Potentia.

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Title: Allicin-Mediated Cell Cycle Regulation Reverses Taxol Resistance in NSCLC: Molecular Insights and Therapeutic Potentia.
Authors: Gao, Xudong1 (AUTHOR), Santhanam, Ramesh kumar2 (AUTHOR), Huang, Zeng3 (AUTHOR), Liu, Mingyue4 (AUTHOR), Hou, Shanbo5 (AUTHOR), Song, Aigang5 (AUTHOR), Ren, Tianshu1 (AUTHOR), Zhao, Qingchun1 (AUTHOR)
Source: Journal of Food Biochemistry. 12/13/2023, p1-14. 14p.
Subjects: Cell cycle regulation, Paclitaxel, Non-small-cell lung carcinoma, Pulmonary nodules, Regulator genes
Abstract: The clinical efficacy of non-small-cell lung cancer (NSCLC) treatment is significantly hindered by Taxol resistance, demanding the exploration of novel approaches to overcome this challenge. Natural products, renowned for their diverse anticancer potential, offer hope, with allicin emerging as a captivating contender. However, the intricate role and underlying mechanisms of allicin in NSCLC Taxol resistance remain largely unexplored. In this extensive investigation, we delve into the impact of allicin on Taxol resistance, meticulously examining both in vitro and in vivo scenarios. Remarkably, allicin effectively curbs the proliferation and migration of A549/Taxol cells while inducing apoptosis. Unraveling the regulatory potential of genes like CDK1 in the cell cycle pathway, allicin demonstrated the ability to arrest cells in the G2/M phase, thus disrupting the cell cycle and heightening Taxol sensitivity. Strikingly, when combined with Taxol, allicin showed the ability to promote Taxol to inhibit tumor growth and reduce lung nodules in tumor-bearing mice, all without significant toxicity. Importantly, allicin's prowess in reversing Taxol resistance via cell cycle regulation sheds light on its potential as a resistance-reversing agent in NSCLC, marking a vital milestone in the quest for natural source therapies. [ABSTRACT FROM AUTHOR]
Copyright of Journal of Food Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Allicin-Mediated Cell Cycle Regulation Reverses Taxol Resistance in NSCLC: Molecular Insights and Therapeutic Potentia.
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  Data: <searchLink fieldCode="DE" term="%22Cell+cycle+regulation%22">Cell cycle regulation</searchLink><br /><searchLink fieldCode="DE" term="%22Paclitaxel%22">Paclitaxel</searchLink><br /><searchLink fieldCode="DE" term="%22Non-small-cell+lung+carcinoma%22">Non-small-cell lung carcinoma</searchLink><br /><searchLink fieldCode="DE" term="%22Pulmonary+nodules%22">Pulmonary nodules</searchLink><br /><searchLink fieldCode="DE" term="%22Regulator+genes%22">Regulator genes</searchLink>
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  Label: Abstract
  Group: Ab
  Data: The clinical efficacy of non-small-cell lung cancer (NSCLC) treatment is significantly hindered by Taxol resistance, demanding the exploration of novel approaches to overcome this challenge. Natural products, renowned for their diverse anticancer potential, offer hope, with allicin emerging as a captivating contender. However, the intricate role and underlying mechanisms of allicin in NSCLC Taxol resistance remain largely unexplored. In this extensive investigation, we delve into the impact of allicin on Taxol resistance, meticulously examining both in vitro and in vivo scenarios. Remarkably, allicin effectively curbs the proliferation and migration of A549/Taxol cells while inducing apoptosis. Unraveling the regulatory potential of genes like CDK1 in the cell cycle pathway, allicin demonstrated the ability to arrest cells in the G2/M phase, thus disrupting the cell cycle and heightening Taxol sensitivity. Strikingly, when combined with Taxol, allicin showed the ability to promote Taxol to inhibit tumor growth and reduce lung nodules in tumor-bearing mice, all without significant toxicity. Importantly, allicin's prowess in reversing Taxol resistance via cell cycle regulation sheds light on its potential as a resistance-reversing agent in NSCLC, marking a vital milestone in the quest for natural source therapies. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Journal of Food Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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      – Type: doi
        Value: 10.1155/2023/9910431
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      – Code: eng
        Text: English
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        PageCount: 14
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      – SubjectFull: Cell cycle regulation
        Type: general
      – SubjectFull: Paclitaxel
        Type: general
      – SubjectFull: Non-small-cell lung carcinoma
        Type: general
      – SubjectFull: Pulmonary nodules
        Type: general
      – SubjectFull: Regulator genes
        Type: general
    Titles:
      – TitleFull: Allicin-Mediated Cell Cycle Regulation Reverses Taxol Resistance in NSCLC: Molecular Insights and Therapeutic Potentia.
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            NameFull: Gao, Xudong
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            NameFull: Santhanam, Ramesh kumar
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            NameFull: Liu, Mingyue
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            NameFull: Hou, Shanbo
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            NameFull: Song, Aigang
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              Text: 12/13/2023
              Type: published
              Y: 2023
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