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载脂肪酸合酶(FASN)siRNA 的 Her-2 靶向 Fab'-免疫脂质体用于乳腺癌细胞的基因沉默。

Fatty Acid Synthase (FASN) siRNA-Encapsulated-Her-2 Targeted Fab'-Immunoliposomes for Gene Silencing in Breast Cancer Cells.

机构信息

Department of Basic Health Sciences, College of Applied Medical Sciences, Qassim University, Al-Qassim, Buraydah, Saudi Arabia.

Department of Pharmaceutics, College of Pharmacy, Qassim University, Al-Qassim, Buraydah, Saudi Arabia.

出版信息

Int J Nanomedicine. 2020 Aug 5;15:5575-5589. doi: 10.2147/IJN.S256022. eCollection 2020.

DOI:10.2147/IJN.S256022
PMID:32801705
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7415462/
Abstract

PURPOSE

The overexpression of Her-2 in 25-30% breast cancer cases and the crosstalk between Her-2 and fatty acid synthase (FASN) establishes Her-2 as a promising target for site-directed delivery. The present study aimed to develop the novel lipid base formulations to target and inhibit the cellular proliferation of Her-2-expressing breast cancer cells through the silencing of FASN. In order to achieve this goal, we prepared DSPC/Chol and DOPE/CHEMS immunoliposomes, conjugated with the anti-Her-2 fab' and encapsulated FASN siRNA against breast cancer cells.

METHODS

We evaluated the size, stability, cellular uptake and internalization of various formulations of liposomes. The antiproliferative gene silencing potential was investigated by the cell cytotoxicity, crystal violet, wound healing and Western blot analyses in Her-2 and Her-2 breast cancer cells.

RESULTS

The data revealed that both nanosized FASN-siRNA-encapsulated liposomes showed significantly higher cellular uptake and internalization with enhanced stability. The cell viability of Her-2 SK-BR3 cells treated with the targeted formulation of DSPC/Chol- and DOPE/CHEMS-encapsulating FASN-siRNA reduced to 30% and 20%, respectively, whereas it was found to be 45% and 36% in MCF-7 cells. The wounds were not only failed to close but they became broader in Her-2 cells treated with targeted liposomes of siRNA. Consequently, the amount of FASN decreased by 80% in SK-BR3 cells treated with non-targeted liposomes and it was 30% and 60% in the MCF-7 cells treated with DSPC/Chol and DOPE/CHEMS liposomes, respectively.

CONCLUSION

In this study, we developed the formulation that targeted Her-2 for the suppression of FASN and, therefore, inhibited the proliferation of breast cancer cells.

摘要

目的

在 25-30%的乳腺癌病例中，Her-2 的过度表达以及 Her-2 与脂肪酸合酶（FASN）之间的串扰使 Her-2 成为靶向给药的有希望的靶点。本研究旨在开发新型脂质基制剂，通过沉默 FASN 靶向和抑制 Her-2 表达的乳腺癌细胞的细胞增殖。为了实现这一目标，我们制备了 DSPC/Chol 和 DOPE/CHEMS 免疫脂质体，与抗 Her-2 fab'缀合，并包封针对乳腺癌细胞的 FASN siRNA。

方法

我们评估了各种脂质体制剂的大小、稳定性、细胞摄取和内化。通过细胞毒性、结晶紫、划痕愈合和 Western blot 分析研究了抗增殖基因沉默的潜力在 Her-2 和 Her-2 乳腺癌细胞中。

结果

数据显示，两种纳米大小的 FASN-siRNA 包封脂质体均表现出更高的细胞摄取和内化，并且稳定性增强。用靶向制剂 DSPC/Chol 和 DOPE/CHEMS 包封 FASN-siRNA 处理的 Her-2 SK-BR3 细胞的细胞活力分别降低至 30%和 20%，而在 MCF-7 细胞中发现为 45%和 36%。用靶向脂质体的 siRNA 处理的 Her-2 细胞的伤口不仅未闭合，反而变得更宽。因此，用非靶向脂质体处理的 SK-BR3 细胞中 FASN 的量减少了 80%，而在用 DSPC/Chol 和 DOPE/CHEMS 脂质体处理的 MCF-7 细胞中分别减少了 30%和 60%。

结论

在这项研究中，我们开发了针对 Her-2 的制剂，用于抑制 FASN，从而抑制乳腺癌细胞的增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/22eaaff713de/IJN-15-5575-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/1857a4e42526/IJN-15-5575-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/839397b9d76d/IJN-15-5575-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/cab1de17893a/IJN-15-5575-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/b96c2948b07e/IJN-15-5575-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/69d941607a3e/IJN-15-5575-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/e2e232560b5c/IJN-15-5575-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/d6598dec9585/IJN-15-5575-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/22eaaff713de/IJN-15-5575-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/1857a4e42526/IJN-15-5575-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/839397b9d76d/IJN-15-5575-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/cab1de17893a/IJN-15-5575-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/b96c2948b07e/IJN-15-5575-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/69d941607a3e/IJN-15-5575-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/e2e232560b5c/IJN-15-5575-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/d6598dec9585/IJN-15-5575-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d4/7415462/22eaaff713de/IJN-15-5575-g0008.jpg

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