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褪黑素对人肝癌 HepG2 细胞的抗增殖作用主要通过细胞周期阻滞和炎症抑制来实现。

Anti-proliferative effect of melatonin in human hepatoma HepG2 cells occurs mainly through cell cycle arrest and inflammation inhibition.

机构信息

Medical Biochemistry Department, Medicine and Clinical Studies Research Institute, National Research Centre, 33 El Bohouth St., Dokki, Giza, 12622, Egypt.

Chemistry of Medicinal Plants Department, and Biology Unit, Central Laboratory for Pharmaceutical and Drug Industries Research Institute, National Research Centre, 33 El Bohouth St., Dokki, Giza, 12622, Egypt.

出版信息

Sci Rep. 2023 Mar 16;13(1):4396. doi: 10.1038/s41598-023-31443-9.

Abstract

Hepatocellular carcinoma (HCC) is the major lethal primary liver malignant worldwide. Although, melatonin has various antitumor bioactivities; there is a requirement for more investigations to elucidate the not discussed effects, and the controversial responses of the treatment with melatonin on targets mediated in HCC. To achieve the aim of the present study, HCC-HepG2 cells were treated with different concentrations of melatonin at various time intervals. The selected minimal proliferation inhibition doses of melatonin were then incubated with cells to examine the arresting effect of melatonin on dividing cells using flow cytometry. Furthermore, the molecular patterns of genes that contributed to apoptosis, drug resistance development, antioxidation, and melatonin crossing were quantified by qRT-PCR. Additionally, the Human inflammation antibody array membrane (40 targets) was used to check the anti-inflammatory effect of melatonin. Our results validated that, melatonin shows anti-proliferative action through preserving cells in G0/G1 phase (P < 0.001) that is associated with a highly significant increase in the expression level of the P53 gene (P < 0.01). On contrary, as a novelty, our data recorded decreases in expression levels of genes involved in the pro-apoptotic pathway; with a significant increase (P < 0.05) in the expression level of an anti-apoptotic gene, Bcl2. Interestingly, we detected observed increases in the expression levels of genes responsible for conferring drug resistance including ABCB1, ABCC1, and ABCC5. Our study proved the anti-inflammatory activity of 1 mM melatonin in HCC-HepG2 cells. Accordingly, we can conclude that melatonin facilitates the anti-proliferation of cells at doses of 1 mM, and 2.5 mM after 24 h. This action is initiated through cell cycle arrest at G0/G1 phase via increasing the expression of P53, but independently on apoptosis. Collectively, melatonin is an effective anti-inflammatory and anti-proliferative promising therapy for the treatment of HCC. However, its consumption should be cautious to avoid the development of drug resistance and provide a better treatment strategy.

摘要

肝细胞癌(HCC)是全球主要的致命原发性肝癌。尽管褪黑素具有多种抗肿瘤生物活性,但仍需要更多的研究来阐明其未被讨论的作用,以及褪黑素对 HCC 中介导靶点的治疗的有争议的反应。为了实现本研究的目的,用不同浓度的褪黑素在不同时间间隔处理 HCC-HepG2 细胞。然后用选择的褪黑素最小增殖抑制剂量孵育细胞,并用流式细胞术检查褪黑素对分裂细胞的阻滞作用。此外,通过 qRT-PCR 定量测定了参与凋亡、耐药发展、抗氧化和褪黑素转运的基因的分子模式。此外,还使用人类炎症抗体阵列膜(40 个靶点)检查褪黑素的抗炎作用。我们的结果验证了褪黑素通过将细胞保持在 G0/G1 期来显示出抗增殖作用(P<0.001),这与 P53 基因表达水平的显著升高(P<0.01)相关。相反,作为一个新颖之处,我们的数据记录了参与促凋亡途径的基因表达水平的降低;抗凋亡基因 Bcl2 的表达水平显著增加(P<0.05)。有趣的是,我们检测到与耐药相关的基因表达水平增加,包括 ABCB1、ABCC1 和 ABCC5。我们的研究证明了 1mM 褪黑素在 HCC-HepG2 细胞中的抗炎活性。因此,我们可以得出结论,褪黑素在 1mM 和 2.5mM 剂量下,在 24 小时后促进细胞增殖。这种作用是通过增加 P53 的表达,在 G0/G1 期引起细胞周期阻滞而启动的,但与凋亡无关。总的来说,褪黑素是一种有效的抗炎和抗增殖的治疗方法,有望用于治疗 HCC。然而,为了避免耐药性的发展,应该谨慎使用其来提供更好的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41fb/10020432/4362da622b84/41598_2023_31443_Fig1_HTML.jpg

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