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纳米载体介导的天然化合物/siRNA 共递用于癌症治疗的研究进展。

Progress in Natural Compounds/siRNA Co-delivery Employing Nanovehicles for Cancer Therapy.

机构信息

Faculty of Engineering and Natural Sciences, Sabanci University, Orta Mahalle, Üniversite Caddesi No. 27, Orhanlı, Tuzla, 34956 Istanbul, Turkey.

Sabanci University Nanotechnology Research and Application Center (SUNUM), Tuzla 34956, Istanbul Turkey.

出版信息

ACS Comb Sci. 2020 Dec 14;22(12):669-700. doi: 10.1021/acscombsci.0c00099. Epub 2020 Oct 23.


DOI:10.1021/acscombsci.0c00099
PMID:33095554
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8015217/
Abstract

Chemotherapy using natural compounds, such as resveratrol, curcumin, paclitaxel, docetaxel, etoposide, doxorubicin, and camptothecin, is of importance in cancer therapy because of the outstanding therapeutic activity and multitargeting capability of these compounds. However, poor solubility and bioavailability of natural compounds have limited their efficacy in cancer therapy. To circumvent this hurdle, nanocarriers have been designed to improve the antitumor activity of the aforementioned compounds. Nevertheless, cancer treatment is still a challenge, demanding novel strategies. It is well-known that a combination of natural products and gene therapy is advantageous over monotherapy. Delivery of multiple therapeutic agents/small interfering RNA (siRNA) as a potent gene-editing tool in cancer therapy can maximize the synergistic effects against tumor cells. In the present review, co-delivery of natural compounds/siRNA using nanovehicles are highlighted to provide a backdrop for future research.

摘要

使用天然化合物(如白藜芦醇、姜黄素、紫杉醇、多西紫杉醇、依托泊苷、阿霉素和喜树碱)进行化疗在癌症治疗中非常重要,因为这些化合物具有出色的治疗活性和多靶向能力。然而,天然化合物的溶解度和生物利用度差限制了它们在癌症治疗中的疗效。为了克服这一障碍,已经设计了纳米载体来提高上述化合物的抗肿瘤活性。尽管如此,癌症治疗仍然是一个挑战,需要新的策略。众所周知,天然产物与基因治疗的联合应用优于单一疗法。将多种治疗剂/小干扰 RNA(siRNA)作为一种有效的基因编辑工具递送至癌症治疗中,可以最大限度地发挥对肿瘤细胞的协同作用。在本综述中,强调了使用纳米载体共递送天然化合物/siRNA,为未来的研究提供了背景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/6ca418fb0e35/co0c00099_0010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/015153e88dc1/co0c00099_0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/511fb3fce3de/co0c00099_0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/39541532d69e/co0c00099_0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/e21bca8e7783/co0c00099_0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/17bd3407d5ed/co0c00099_0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/2c89238ed5b3/co0c00099_0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/65a8d15016fb/co0c00099_0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/a49b21a495cb/co0c00099_0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/6aba48b3a430/co0c00099_0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/6ca418fb0e35/co0c00099_0010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/015153e88dc1/co0c00099_0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/511fb3fce3de/co0c00099_0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/39541532d69e/co0c00099_0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/e21bca8e7783/co0c00099_0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/17bd3407d5ed/co0c00099_0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/2c89238ed5b3/co0c00099_0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/65a8d15016fb/co0c00099_0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/a49b21a495cb/co0c00099_0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/6aba48b3a430/co0c00099_0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3f/8015217/6ca418fb0e35/co0c00099_0010.jpg

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本文引用的文献

[1]
Brusatol suppresses STAT3-driven metastasis by downregulating epithelial-mesenchymal transition in hepatocellular carcinoma.

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