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原花青素在体外可降低全球诊断率最高的几种癌症中的细胞功能。

Proanthocyanidins reduce cellular function in the most globally diagnosed cancers in vitro.

作者信息

Albogami Sarah

机构信息

Department of Biotechnology, Faculty of Science, Taif University, Taif, Makkah, Kingdom of Saudi Arabia.

出版信息

PeerJ. 2020 Sep 15;8:e9910. doi: 10.7717/peerj.9910. eCollection 2020.

DOI:10.7717/peerj.9910
PMID:32983646
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7500326/
Abstract

BACKGROUND

Growing evidence indicates that proanthocyanidins (PACs) may be effective in treating and preventing various cancers. The fundamental mechanism of PACs inhibiting the proliferation at cellular and molecular levels in most of the cancer types remains unclear.

OBJECTIVE

The anticancer efficacy of PACs was investigated in vitro using three human cancer cell lines: human colorectal adenocarcinoma (HT-29), human breast carcinoma (MCF-7), and human prostatic adenocarcinoma (PC-3).

METHODS

Cytotoxicity was evaluated by MTT assay, while cell proliferation was measured by trypan blue exclusion method. Cell migration was measured by wound healing assay, and DAPI staining was used to evaluate apoptotic nucleus morphology. RT-PCR was used to analyze the expression of and , and caspase enzyme activity assay was measured by caspase colorimetric assay.

RESULTS

PACs could inhibit both cellular viability and proliferation in a concentration- and time-dependent fashion in all investigated cells. Further, all tested cells showed similarly decreased migration after 24- and 48-h PAC treatment. We observed increased apoptotic nucleus morphology in treated cells ( ≤ 0.01). expression significantly increased in HT-29 ( < 0.01), PC-3( < 0.01), and MCF-7 ( < 0.05) cells, while expression significantly declined ( < 0.05). Caspase activities were significantly increased in all tested cancer cell lines after 24-h PAC treatment.

CONCLUSION

PACs may have potential therapeutic properties against colorectal, breast, and prostate cancer.

摘要

背景

越来越多的证据表明,原花青素(PACs)可能对治疗和预防各种癌症有效。在大多数癌症类型中,PACs在细胞和分子水平上抑制增殖的基本机制仍不清楚。

目的

使用三种人类癌细胞系:人结肠腺癌(HT-29)、人乳腺癌(MCF-7)和人前列腺腺癌(PC-3),在体外研究PACs的抗癌功效。

方法

通过MTT法评估细胞毒性,同时通过台盼蓝排斥法测量细胞增殖。通过伤口愈合试验测量细胞迁移,并使用DAPI染色评估凋亡细胞核形态。RT-PCR用于分析 和 的表达,通过半胱天冬酶比色法测量半胱天冬酶酶活性。

结果

PACs能够以浓度和时间依赖性方式抑制所有研究细胞的细胞活力和增殖。此外,在24小时和48小时的PAC处理后,所有测试细胞的迁移均同样减少。我们观察到处理后的细胞中凋亡细胞核形态增加( ≤ 0.01)。HT-29( < 0.01)、PC-3( < 0.01)和MCF-7( < 0.05)细胞中的 表达显著增加,而 表达显著下降( < 0.05)。在24小时的PAC处理后,所有测试癌细胞系中的半胱天冬酶活性均显著增加。

结论

PACs可能对结直肠癌、乳腺癌和前列腺癌具有潜在的治疗特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/4a3b5cf779bc/peerj-08-9910-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/34a7cd84b8af/peerj-08-9910-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/db0c4ba42919/peerj-08-9910-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/dfb83e5994c6/peerj-08-9910-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/c46d0e333da9/peerj-08-9910-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/839669b57d9b/peerj-08-9910-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/492c72494cca/peerj-08-9910-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/f7bdd3a7b32a/peerj-08-9910-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/48d41354671b/peerj-08-9910-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/cc71639296c5/peerj-08-9910-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/4a3b5cf779bc/peerj-08-9910-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/34a7cd84b8af/peerj-08-9910-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/db0c4ba42919/peerj-08-9910-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/dfb83e5994c6/peerj-08-9910-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/c46d0e333da9/peerj-08-9910-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/839669b57d9b/peerj-08-9910-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/492c72494cca/peerj-08-9910-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/f7bdd3a7b32a/peerj-08-9910-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/48d41354671b/peerj-08-9910-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/cc71639296c5/peerj-08-9910-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a298/7500326/4a3b5cf779bc/peerj-08-9910-g010.jpg

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