Application of SIRT1 expression interfering agent in preparation of medicine for inhibiting self renewal of liver cancer stem cell agent

A technology for inhibiting liver cancer and stem cells, applied in the field of chemistry, can solve problems such as unreported, and achieve the effect of prolonging survival time and delaying tumor growth

Active Publication Date: 2014-04-30
THE FIRST AFFILIATED HOSPITAL OF THIRD MILITARY MEDICAL UNIVERSITY OF PLA
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

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Problems solved by technology

At present, the research on SIRT1 in stem cells mainly focuses on mouse and human embryonic stem cells and human hematopoietic stem cells, but SIRT1 regulates the expression of solid tumors, especially in liver cancer stem cells, and its role and molecular mechanism have not been reported yet.

Method used

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  • Application of SIRT1 expression interfering agent in preparation of medicine for inhibiting self renewal of liver cancer stem cell agent
  • Application of SIRT1 expression interfering agent in preparation of medicine for inhibiting self renewal of liver cancer stem cell agent
  • Application of SIRT1 expression interfering agent in preparation of medicine for inhibiting self renewal of liver cancer stem cell agent

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Embodiment Construction

[0030] The preferred embodiments of the present invention will be described in detail below with reference to the accompanying drawings. For the experimental methods that do not indicate the specific conditions in the examples, usually follow the conventional conditions, such as the conditions described in the Molecular Cloning Experiment Guide (Third Edition, J. Sambrook et al.), Shan et al.2012, hepatology, 56 : Conditions described in 1014-1014 or as recommended by the manufacturer.

[0031] The liver cancer stem cell model used in the present invention was constructed by our laboratory. The model contains a lentiviral expression vector (Nanog / GFP reporter system) constructed by the Nanog promoter regulating the GFP reporter gene. For the construction method, see Shan et al.2012, hepatology, 56: 1014-1014; Lv-sh-Scramble plasmid and Lv-sh-SIRT1 plasmid, adenovirus vector AD-GFP were constructed by our laboratory, see Shan et al.2012, Hepatology, 56: 1014-1014; HEK293 cells ...

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Abstract

The invention belongs to the field of chemistry, particularly discloses application of SIRT1 expression interfering agent in preparation of medicine for inhibiting self renewal of liver cancer stem cell. The self renewal of liver cancer stem cells is inhibited by inhibiting SIRT1 expression in liver cancer stem cells to remarkably reduce proliferation capacity, cloning capacity and balling capacity of liver cancer stem cells, so that the SIRT1 expression interfering agent can be used for preparing medicaments for targeting treatment of liver cancer.

Description

technical field [0001] The invention belongs to the field of chemistry, and particularly relates to the application of a reagent for interfering with SIRT1 expression in the preparation of a drug for inhibiting the self-renewal of liver cancer stem cells. Background technique [0002] Tumor is a complex disease caused by genetic changes or epigenetic mutations. Tumor occurrence and evolution are a complex multi-step process. In recent years, studies have found that there is a small group of stem cell-like tumor cell subsets in tumors, which have the ability to initiate tumors, so they are called cancer stem cells (Cancer Stem Cells, CSCs) or tumor initiating cells (Tumor Initiating Cells, TICs). So far, cancer stem cells have been isolated and identified from at least 30 common tumors, including liver cancer, breast cancer, colorectal cancer, glioma, lung cancer, prostate cancer, melanoma, and leukemia. Therefore, the molecular regulation mechanism of CSCs and its mechanis...

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): A61K48/00A61P35/00
Inventor 钱程刘丽梅刘春刚沈俊杰单娟娟
Owner THE FIRST AFFILIATED HOSPITAL OF THIRD MILITARY MEDICAL UNIVERSITY OF PLA
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