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明胶基水凝胶中环状磷酸脂酸的释放抑制结肠癌细胞的生长和迁移。

Release of cyclic phosphatidic acid from gelatin-based hydrogels inhibit colon cancer cell growth and migration.

机构信息

Department of Integrative Physiology & Bio-System Control, Shinshu University School of Medicine , 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan.

出版信息

Sci Rep. 2012;2:687. doi: 10.1038/srep00687. Epub 2012 Sep 24.

DOI:10.1038/srep00687
PMID:23008752
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3449289/
Abstract

Microparticle and nanoparticle formulations are widely used to improve the bioavailability of low-solubility drugs and as vehicles for organ- and tissue-specific targeted drug delivery. We investigated the effect of a novel, controlled-release form of a bioactive lipid, cyclic phosphatidic acid (cPA), on human colon cancer cell line functions. We encapsulated cPA in gelatin-based hydrogels and examined its ability to inhibit the viability and migration of HT-29 and DLD-1 cells in vitro and the LPA-induced activity of the transcription factor peroxisome proliferator-activated receptor gamma (PPARγ). The hydrogel delivery system prolonged cPA release into the culture medium. Accordingly, cPA-hydrogel microspheres substantially inhibited LPA-induced PPARγ activity and cell growth and migration compared with that of cells cultured with cPA alone. Thus, hydrogel microspheres are a potential system for stable and efficient delivery of bioactive lipids such as cPA and may offer a new strategy for targeted colon cancer treatment.

摘要

微粒体和纳米粒子制剂被广泛用于提高低溶解度药物的生物利用度,并作为器官和组织特异性靶向药物递送的载体。我们研究了新型生物活性脂质环磷酸脂酸(cPA)的控释制剂对人结肠癌细胞系功能的影响。我们将 cPA 包裹在明胶基水凝胶中,并研究了其在体外抑制 HT-29 和 DLD-1 细胞活力和迁移以及 LPA 诱导转录因子过氧化物酶体增殖物激活受体γ(PPARγ)活性的能力。水凝胶递送系统将 cPA 释放到培养基中延长。因此,与单独用 cPA 培养的细胞相比,cPA-水凝胶微球大大抑制了 LPA 诱导的 PPARγ 活性和细胞生长及迁移。因此,水凝胶微球是一种稳定高效递送生物活性脂质如 cPA 的潜在系统,可能为结肠癌的靶向治疗提供新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/851dbdb19eda/srep00687-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/6ec976aab6ba/srep00687-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/f32c325cd67b/srep00687-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/7e7de940136b/srep00687-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/928b47e697c3/srep00687-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/851dbdb19eda/srep00687-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/6ec976aab6ba/srep00687-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/f32c325cd67b/srep00687-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/7e7de940136b/srep00687-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/928b47e697c3/srep00687-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0fe/3449289/851dbdb19eda/srep00687-f5.jpg

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本文引用的文献

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The PPARgamma antagonist T0070907 suppresses breast cancer cell proliferation and motility via both PPARgamma-dependent and -independent mechanisms.PPARγ 拮抗剂 T0070907 通过 PPARγ 依赖和非依赖机制抑制乳腺癌细胞增殖和迁移。
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