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穿心莲内酯是一种通过胆固醇生物合成途径克服雌激素受体阳性乳腺癌耐药性的替代治疗方法。

Andrographolide is an Alternative Treatment to Overcome Resistance in ER-Positive Breast Cancer via Cholesterol Biosynthesis Pathway.

作者信息

Rajaratinam Harishini, Nafi Siti Norasikin Mohd

机构信息

Department of Pathology, School of Medical Sciences, Universiti Sains Malaysia, Kota Bharu, Kelantan, Malaysia.

Department of Pathology, Hospital Universiti Sains Malaysia, Kota Bharu, Kelantan, Malaysia.

出版信息

Malays J Med Sci. 2019 Sep;26(5):6-20. doi: 10.21315/mjms2019.26.5.2. Epub 2019 Nov 4.

DOI:10.21315/mjms2019.26.5.2
PMID:31728115
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6839656/
Abstract

Oestrogen receptor (ER)-positive breast cancer is one of the common forms of breast cancer affecting women worldwide. ER-positive breast cancer patients are subjected to anti-oestrogen therapy such as selective oestrogen receptor modulator (SERM) and aromatase inhibitors (AIs). Recently, the emergence of resistance to anti-oestrogen treatment is under intensive focus. The different mechanisms postulated to explain the occurrence of resistance in ER-positive breast cancer treatment include the loss of ER function and the crosstalk between signalling pathways in cancer cells. Recent literature highlighted that the cholesterol biosynthesis pathway acts as a novel mechanism underlying resistance to oestrogen deprivation. The present study aimed to highlight the role of cholesterol biosynthesis in anti-oestrogen treatment resistance, putatively suggesting an alternative plant-based treatment using andrographolide from . The hypolipidaemic effect of andrographolide can be utilised to prevent the resistance in the treatment of ER-positive breast cancer contributed by cholesterol biosynthesis.

摘要

雌激素受体(ER)阳性乳腺癌是影响全球女性的常见乳腺癌形式之一。ER阳性乳腺癌患者会接受抗雌激素治疗,如选择性雌激素受体调节剂(SERM)和芳香化酶抑制剂(AI)。最近,抗雌激素治疗耐药性的出现受到了密切关注。为解释ER阳性乳腺癌治疗中耐药性产生而提出的不同机制包括ER功能丧失以及癌细胞信号通路之间的相互作用。最近的文献强调,胆固醇生物合成途径是雌激素剥夺耐药性的一种新机制。本研究旨在突出胆固醇生物合成在抗雌激素治疗耐药性中的作用,推测性地提出使用穿心莲内酯进行基于植物的替代治疗。穿心莲内酯的降血脂作用可用于预防胆固醇生物合成导致的ER阳性乳腺癌治疗中的耐药性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/71c21281f2ec/02mjms26052019_ra1f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/5280b84ea504/02mjms26052019_ra1f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/cdd3785ca0ea/02mjms26052019_ra1f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/b210bc4124b9/02mjms26052019_ra1f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/8a10eef2defd/02mjms26052019_ra1f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/bc7a9c017f2d/02mjms26052019_ra1f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/71c9b3c128d6/02mjms26052019_ra1f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/3c67a7a413af/02mjms26052019_ra1f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/71c21281f2ec/02mjms26052019_ra1f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/5280b84ea504/02mjms26052019_ra1f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/cdd3785ca0ea/02mjms26052019_ra1f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/b210bc4124b9/02mjms26052019_ra1f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/8a10eef2defd/02mjms26052019_ra1f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/bc7a9c017f2d/02mjms26052019_ra1f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/71c9b3c128d6/02mjms26052019_ra1f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/3c67a7a413af/02mjms26052019_ra1f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7b1/6839656/71c21281f2ec/02mjms26052019_ra1f8.jpg

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Mol Pharm. 2018 Apr 2;15(4):1618-1626. doi: 10.1021/acs.molpharmaceut.7b01164. Epub 2018 Mar 2.
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BMJ. 2016 Jun 1;353:i3108. doi: 10.1136/bmj.i3108.
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