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Journal of Zhejiang University SCIENCE B

ISSN 1673-1581(Print), 1862-1783(Online), Monthly

Luteolin suppresses oral carcinoma 3 (OC3) cell growth and migration via modulating polo-like kinase 1 (PLK1) expression and cellular energy metabolism

Abstract: Oral squamous cell carcinoma (OSCC) is a prevalent malignant tumor affecting the head and neck region (Leemans et al., 2018). It is often diagnosed at a later stage, leading to a poor prognosis (Muzaffar et al., 2021; Li et al., 2023). Despite advances in OSCC treatment, the overall 5-year survival rate of OSCC patients remains alarmingly low, falling below 50% (Jehn et al., 2019; Johnson et al., 2020). According to statistics, only 50% of patients with oral cancer can be treated with surgery. Once discovered, it is more frequently at an advanced stage. In addition, owing to the aggressively invasive and metastatic characteristics of OSCC, most patients die within one year of diagnosis. Hence, the pursuit of novel therapeutic drugs and treatments to improve the response of oral cancer to medication, along with a deeper understanding of their effects, remains crucial objectives in oral cancer research (Johnson et al., 2020; Bhat et al., 2021; Chen et al., 2023; Ruffin et al., 2023).

Key words: luteolin, oral cancer, proliferation, P53-PLK1 signaling, energy metabolism, anti-cancer

Chinese Summary  <24> 木犀草素通过调节PLK1表达和细胞能量代谢抑制口腔癌细胞OC3的生长和迁移

高鹏飞1,2,张文涛1,林宇杰3,卢睿杰3,楼子健3,卢刚4,潘若浪4,陈云芳1,2
1浙江省人民医院,杭州医学院附属人民医院口腔科整形重建外科中心,中国杭州市,310014
2蚌埠医学院口腔医学院,中国蚌埠市,233030
3温州医科大学附属第二临床医学院,中国温州市,325035
4浙江省细胞药物与应用技术研究重点实验室,中国杭州市,311122
摘要:尽管木犀草素的抗癌作用已在多种肿瘤模型中报道,但关于其在口腔癌中的作用研究鲜少。本研究探讨了木犀草素对口腔癌细胞OC3生长和迁移的影响及其机制。结果表明,木犀草素能够抑制或下调OC3细胞的增殖、细胞周期以及p53-Ser15(P)和polo样激酶1(PLK1)蛋白水平。耗氧率(OCR)和胞外酸化率(ECAR)水平以及ATP产量也显著降低。Transwell试验进一步证实OC3细胞的迁移能力会受到木犀草素的影响。综上,本研究发现木犀草素能抑制口腔癌细胞OC3的增殖,其机制可能与p53-PLK1信号传导下调和细胞能量代谢降低有关。

关键词组:木犀草素;口腔癌;增殖;p53-PLK1信号通路;能量代谢;抗癌


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DOI:

10.1631/jzus.B2300200

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On-line Access:

2024-08-27

Received:

2023-10-17

Revision Accepted:

2024-05-08

Crosschecked:

2023-12-12

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