Bismuth oxide nanoparticles inhibit HCT116 colorectal cancer cells by inducing apoptosis, cell cycle arrest and ROS production

IF 3.7 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Process Biochemistry Pub Date : 2024-11-15 DOI:10.1016/j.procbio.2024.11.017

Yongjing Hu , Ying Yin , Jiayan Shi , Ali Bahadur , Kamyar Shameli , Chenxiao Zheng , Xiaodong Zhang , Sin-Yeang Teow

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引用次数: 0

Abstract

Nanoparticles (NPs) have recently gained traction for anticancer use. Colorectal cancer (CRC) is one of the most common cancer types in the world, but only a few studies have previously reported the anticancer action of Bi₂O₃ NPs towards CRC, and the underlying mechanisms are not well understood. In this study, 1 mg/ml Bi₂O₃ NPs showed 60 % and 8 % inhibition in HCT116 and HT-29 cells, respectively. In the HCT116 spheroid, Bi₂O₃ NPs showed reduced inhibition of 27 % at 1 mg/ml due to the more stringent tissue architecture. Both CRC cells showed successful internalization of Bi₂O₃ NPs through flow cytometry and ICP-MS. The NPs mainly killed HCT116 cells by inducing late-stage apoptosis (∼17 %). In addition, Bi₂O₃ NPs also induced S and G2/M cell cycle arrest (∼4 % and ∼10 %) by targeting CDK2 protein in HCT116 cells. In HT-29 cells, Bi₂O₃ NPs did not trigger apoptosis but induced ∼22 % G2/M cell cycle arrest. Bi₂O₃ NPs also induced ROS production, and potently inhibited the cell migration. 300 μg/ml Bi₂O₃ NPs also exhibited anti-angiogenic action in the angiogenesis assay. In conclusion, the present study highlights the potential anticancer effect of Bi₂O₃ NPs towards CRC, and further investigation is warranted to improve the biocompatibility, targeted selectivity, and tumor-penetrating capacity.

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氧化铋纳米颗粒通过诱导细胞凋亡、细胞周期停滞和产生 ROS 抑制 HCT116 大肠癌细胞

最近，纳米粒子（NPs）在抗癌方面的应用越来越受到关注。结直肠癌（CRC）是世界上最常见的癌症类型之一，但此前只有少数研究报道了 Bi2O3 NPs 对 CRC 的抗癌作用，而且对其潜在机制还不甚了解。在这项研究中，1 毫克/毫升的 Bi2O3 NPs 对 HCT116 和 HT-29 细胞的抑制率分别为 60% 和 8%。在 HCT116 球形细胞中，由于组织结构更为严格，1 毫克/毫升的 Bi2O3 NPs 的抑制率降低了 27%。通过流式细胞仪和 ICP-MS 检测，两种 CRC 细胞都显示出 Bi2O3 NPs 的成功内化。NPs 主要通过诱导晚期细胞凋亡杀死 HCT116 细胞（17%）。此外，Bi2O3 NPs 还通过靶向 CDK2 蛋白诱导 HCT116 细胞的 S 和 G2/M 细胞周期停滞（4 % 和 10 %）。在 HT-29 细胞中，Bi2O3 NPs 未引发细胞凋亡，但诱导了 22% 的 G2/M 细胞周期停滞。Bi2O3 NPs 还能诱导 ROS 生成，并有效抑制细胞迁移。在血管生成试验中，300 μg/ml Bi2O3 NPs 还具有抗血管生成作用。总之，本研究强调了 Bi2O3 NPs 对 CRC 的潜在抗癌作用，并认为有必要进一步研究其生物相容性、靶向选择性和肿瘤穿透能力。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Process Biochemistry 生物-工程：化工

CiteScore

8.30

自引率

4.50%

发文量

374

审稿时长

53 days

期刊介绍： Process Biochemistry is an application-orientated research journal devoted to reporting advances with originality and novelty, in the science and technology of the processes involving bioactive molecules and living organisms. These processes concern the production of useful metabolites or materials, or the removal of toxic compounds using tools and methods of current biology and engineering. Its main areas of interest include novel bioprocesses and enabling technologies (such as nanobiotechnology, tissue engineering, directed evolution, metabolic engineering, systems biology, and synthetic biology) applicable in food (nutraceutical), healthcare (medical, pharmaceutical, cosmetic), energy (biofuels), environmental, and biorefinery industries and their underlying biological and engineering principles.