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标准化组分使SiHa细胞停滞于G1/S期，并通过上调p53诱导细胞凋亡。

Standardized Fraction Arrested SiHa Cells at G1/S and Induced Apoptosis via Upregulation of p53.

作者信息

Nik Zainuddin Nik Aina Syazana, Muhammad Hussin, Nik Hassan Nik Fakhuruddin, Othman Nor Hayati, Zakaria Yusmazura

机构信息

Biomedicine Programme, School of Health Sciences, Universiti Sains Malaysia (USM) Health Campus, 16150 Kota Bharu, Kelantan, Malaysia.

Toxicology and Pharmacology Unit, Herbal Medicine Research Centre, Institute for Medical Research (IMR), 50588 Kuala Lumpur, Malaysia.

出版信息

J Pharm Bioallied Sci. 2020 Nov;12(Suppl 2):S768-S776. doi: 10.4103/jpbs.JPBS_262_19. Epub 2020 Nov 5.

DOI:10.4103/jpbs.JPBS_262_19
PMID:33828376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8021054/
Abstract

INTRODUCTION

Cervical cancer is a leading cause of death in women. Current cancer treatment comes with side effects. has been known traditionally to treat cancer. This study was aimed to characterize standardized fraction (SF1) and to investigate its anticancer mechanism against SiHa cells.

MATERIALS AND METHODS

SF1 was produced by optimized methodology for bioassay-guided fractionation. Fourier transform infrared (FTIR) spectroscopy and liquid chromatography-mass spectrometry (LC-MS) were carried out to characterize the SF1. SF1 was screened for cytotoxicity activity toward HeLa, SiHa, and normal cells (NIH) cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. The anticancer mechanism of SF1 was evaluated toward SiHa cells, which showed highest cytotoxicity toward SF1 treatment. The mechanism includes cell cycle progression and protein expression, which was detected using specific antibody-conjugated fluorescent dye, p53-FITC, by flow cytometry.

RESULTS

Major constituents of SF1 were alkaloids with amines as functional group. SF1 showed highest cytotoxic activity against SiHa (half-maximal inhibitory concentration [IC] < 10 µg/mL) compared to HeLa cells. Cytoselectivity of SF1 was observed with no IC detected on normal NIH cells. On flow cytometry analysis, SF1 was able to induce apoptosis on SiHa cells by arresting cell cycle at G1/S and upregulation of p53 protein.

CONCLUSION

SF1 showed anticancer activity by inducing apoptosis through arrested G1/S cell cycle checkpoint-mediated mitochondrial pathway.

摘要

引言

宫颈癌是女性死亡的主要原因。目前的癌症治疗伴有副作用。传统上已知[此处原文缺失关键信息]可治疗癌症。本研究旨在表征标准化组分（SF1）并研究其对SiHa细胞的抗癌机制。

材料与方法

SF1通过生物测定导向分级分离的优化方法制备。采用傅里叶变换红外（FTIR）光谱和液相色谱 - 质谱（LC - MS）对SF1进行表征。通过3 -（4,5 - 二甲基噻唑 - 2 - 基）- 2,5 - 二苯基溴化四氮唑（MTT）法筛选SF1对HeLa、SiHa和正常细胞（NIH细胞）的细胞毒性活性。对SF1治疗表现出最高细胞毒性的SiHa细胞评估其抗癌机制。该机制包括细胞周期进程和蛋白质表达，通过使用特异性抗体偶联荧光染料p53 - FITC的流式细胞术进行检测。

结果

SF1的主要成分是带有胺作为官能团的生物碱。与HeLa细胞相比，SF1对SiHa细胞表现出最高的细胞毒性活性（半数最大抑制浓度[IC]<10μg/mL）。观察到SF1具有细胞选择性，在正常NIH细胞上未检测到IC。流式细胞术分析表明，SF1能够通过使细胞周期停滞在G1/S期并上调p53蛋白诱导SiHa细胞凋亡。

结论

SF1通过G1/S细胞周期检查点介导的线粒体途径阻滞诱导凋亡表现出抗癌活性。

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