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A tumor and material technology, applied in the direction of anti-tumor drugs, drug combinations, pharmaceutical formulations, etc., can solve problems such as unclear mechanisms
Inactive Publication Date: 2011-02-23
BEIJING NORMAL UNIVERSITY
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However, it has also been found that some tumor cells ar
Method used
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Embodiment 1
[0095] Example 1. Mechanism of tumor cell resistance to HDACi
[0096] 1. HDACi induces the expression of ATX in tumor cells
[0097] (1) In order to detect whether the expression of ATX in tumor cells is subject to epigenetic modification, colon cancer SW480 cells that do not express ATX were treated with methylase inhibitor (Aza) and histone deacetylase inhibitor (TSA).
[0098] Culture SW480 cells to monolayer (about 70% full), add TSA, treat for 24 hours, use Trizol to lyse the cells, extract RNA; use RT-PCR to detect ATX mRNA expression.
[0099] Set up the following treatment groups:
[0100] Aza-TSA-: No drug added.
[0101] Aza+TSA-: Aza (5 μM) was added without TSA.
[0102] Aza-TSA+: add TSA (100nM) without adding Aza.
[0103] Aza+TSA+: add Aza (5μM), add TSA (100nM).
[0104] Results: TSA can induce ATX expression ( figure 1 a). Aza does not induce ATX expression. It shows that the regulation of ATX expression in tumor cells is not regulated by methylation,...
Embodiment 2
[0199] Example 2. Use of ATX-LPA signaling pathway inhibitor BrP-LPA combined with HDACi medication to improve the ability of HDACi to kill tumors
[0202] SW480 cells were pretreated with BrP-LPA for 1 hour. In the absence of lipid molecules, LPC or LPA, SW480 cells were treated with TSA for 24 hours to detect tumor cell apoptosis.
[0203] The experiment set up the following groups:
[0204] BrP-LPA-TSA-Vehicle+: Add Vehicle without drug treatment.
[0205] BrP-LPA+TSA-Vehicle+: Treat with BrP-LPA (10 μM), add Vehicle.
[0206] BrP-LPA-TSA+Vehicle+: Treat with TSA (250nM), add Vehicle.
[0207] BrP-LPA+TSA+Vehicle+: Treat with BrP-LPA (10μM) and TSA (250nM), add Vehicle.
[0208] BrP-LPA-TSA-LPC+: No drug treatment, ...
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Abstract
The invention discloses a medicament for treating tumors. The medicament consists of a histone deacetylase inhibitor and a lysophosphatidic acid suppressant, wherein the lysophosphatidic acid suppressant is a substance for inhibiting lysophosphatidic acid from bonding with a lysophosphatidic acid receptor or a substance for inhibiting the lysophosphatidic acid from generating. The medicament indicates that the histone deacetylase inhibitor (HDACi) can up-regulate autotaxin (ATX) expression by inhibiting the activity of HDAC3 and HDAC7 in multiple tumor cells. The ATX generated by the induction of the HDACi generates the lysophosphatidic acid (LPA) by catalyzing lysophosphatidyl choline (LPC) and weakens the killing effect of the HDACi on the tumor cells. If the ATX expression is inhibited by a ribonucleic acid interference (RNAi) method or bromophosphonate-lysophosphatidic acid (BrP-LPA) serving as an ATX-LPA signal channel inhibitor is added to block an ATX-LPA signal, the killing effect of the HDACi on the tumor cells can be enhanced further. The study of the invention provides a new concept for treating the tumors by combing the lysophosphatidic acid suppressant and the HDACi. The medicament has wide application prospects in the treatment of the tumors.
Description
technical field [0001] The invention relates to a medicine for treating tumors. Background technique [0002] The histone deacetylase (HDAC) family consists of 18 members divided into four subfamilies. Among them, members of family I are localized in the nucleus, and members of family Π can shuttle between cytoplasm and nucleus. HDAC can also regulate the acetylation of many proteins in cells except histones. [0003] Histone deacetylase inhibitors (HDACi) are anti-tumor drugs that have been widely concerned and applied in recent years. HDACi can kill tumors by various means such as blocking cell cycle progression, inducing differentiation and apoptosis. Researchers have found that HDACi induces the expression of many pro-apoptotic genes in tumor cells, leading to tumor cell death. These HDACi also lead to the expression of death receptors and their ligands in tumor cells, whereas these genes are not upregulated by HDACi in normal cells. More than ten kinds of HDACi hav...
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