Inhibitor for hepatoma carcinoma cell and application to aspect of inhibiting tumor growth thereof

A technology of liver cancer cells and inhibitors, which is applied in the directions of anti-tumor drugs, medical preparations containing active ingredients, and pharmaceutical formulas, can solve problems such as unclearness and achieve the effect of inhibiting growth

Active Publication Date: 2013-02-27
SHANGHAI INST OF ONCOLOGY
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0007] However, to date, whether the combination of PPARγ agonists and AKT inhibitors can effectively target liver tumor-initiating cells to inhibit tumor growth remains unclear.

Method used

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  • Inhibitor for hepatoma carcinoma cell and application to aspect of inhibiting tumor growth thereof
  • Inhibitor for hepatoma carcinoma cell and application to aspect of inhibiting tumor growth thereof
  • Inhibitor for hepatoma carcinoma cell and application to aspect of inhibiting tumor growth thereof

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0049] Negative feedback regulation between NOX2-induced ROS formation and AKT activation in PPARγ agonist-treated liver cancer cells

[0050] (1) The effect of PPARγ agonists on reactive oxygen species in liver cancer cells detected by flow cytometry, only Huh7 and SK-Hep1 cells are used as examples, but the application to other liver cancer cell lines is not limited

[0051] Huh7 and SK-Hep1 cells were incubated at 37°C, 5% CO 2 and saturated humidity conditions, the cell maintenance medium is DMEM high-glucose medium, including 10% fetal bovine serum, 100 μg / ml streptomycin and 100U / ml penicillin. After the cells adhered to the wall, they were all replaced with DMEM high-glucose culture medium containing 1% fetal bovine serum, and the following reagents were added to the culture medium: 15d-PGJ 2 or free radical scavengers NAC or DMSO.

[0052] in,

[0053] Treatment group 1 alone: ​​adding 15d-PGJ 2 (0.5 μg / ml);

[0054] Single treatment group 2: adding free radic...

Embodiment 2

[0095] PPARγ agonists and AKT inhibitors synergistically inhibit the growth and stemness phenotype of hepatocellular carcinoma cells

[0096] (1), PPARγ agonist 15d-PGJ 2 The effect of the combination with the AKT inhibitor tricilibine on the apoptosis of liver cancer cells, only Huh7 cells are used as an example, but it is not limited to the application of other liver cancer cell lines

[0097] Huh7 cells were incubated at 37°C, 5% CO 2 and saturated humidity conditions, the cell maintenance medium is DMEM high-glucose medium, containing 10% fetal bovine serum, 100 μg / ml streptomycin and 100U / ml penicillin. After the cells adhere to the wall, change to DMEM high-glucose culture medium containing 1% fetal bovine serum, and add the following reagents to the culture medium: 15d-PGJ 2 , tricilibine or DMSO.

[0098] in,

[0099] Treatment group 1 alone: ​​adding 15d-PGJ 2 (0.5 μg / ml);

[0100] Single treatment group 2: adding tricitribine (10μM);

[0101] Single tr...

Embodiment 3

[0145] PPARγ agonists and AKT inhibitors synergistically suppress tumor growth

[0146] (1) The effect of PPARγ agonist rosiglitazone and AKT inhibitor triciribine synergistically on tumor growth, only Huh7 cells are used as an example, but the application is not limited to other liver cancer cell lines

[0147] The Huh7 cells stably expressing green fluorescent protein (GFP) were normally cultured in vitro, and the Huh7 cells in the logarithmic growth phase were digested with trypsin, washed twice with PBS, and then the concentration of Huh7 cells was adjusted to 2×10 with PBS. 7 cells / ml, each nude mouse was subcutaneously injected with 100 μl, and the administration began 4 days after subcutaneous tumor bearing, the specific administration method was as follows Figure 3A As shown, they were divided into 4 groups: control group, rosiglitazone treatment group (100mg / kg / day, intragastric administration), triciribine treatment group (1mg / kg / day, intraperitoneal administrat...

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PUM

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Abstract

The invention discloses an inhibitor for a hepatoma carcinoma cell. The inhibitor for the hepatoma carcinoma cell comprises a PPAR (Peroxisome Proliferator Activated Receptor) gamma agonist and AKT inhibitor triciribine, wherein the PPAR gamma agonist is rosiglitazone or 15d-PGJ2; the mass ratio of the PPAR gamma agonist rosiglitazone to the AKT inhibitor triciribine is 100:1; and the mass mole ratio of the PPAR gamma agonist 15d-PGJ2 to the AKT inhibitor triciribine is 1g:(20-100)mu.mol. The inhibitor for the hepatoma carcinoma cell provided by the invention can effectively inhibit the initial cell subset of the HCC (Hepatocellular Carcinoma) tumor and effectively inhibit the tumor growth. A possible effective therapeutic strategy is supplied to the clinic treatment for the HCC.

Description

technical field [0001] The invention relates to an inhibitor of tumor cells, especially an inhibitor of liver cancer cells and its application in inhibiting tumor growth. Background technique [0002] Hepatocellular carcinoma (HCC) is the fifth most common malignant tumor worldwide, and it is the third most lethal malignant tumor due to its resistance to chemotherapy and high recurrence and metastasis after surgery. In recent years, more and more studies have proved that the occurrence of HCC may originate from a group of stem cell subsets, which are called tumor-initiating cells (TICs) or cancer stem cells (cancer stem cells). cells). This population of cells expresses specific surface markers and is characterized by self-renewal, differentiation, tumor formation, and chemotherapy resistance. Although sorafenib has been used in the targeted therapy of HCC, its inhibitory effect on tumors and the survival rate of liver cancer patients are not very good. Therefore, if a th...

Claims

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Application Information

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IPC IPC(8): A61K45/06A61K31/4439A61K31/7064A61K31/5575A61P35/00
Inventor 刘永忠刘兰兰杨兆娟
Owner SHANGHAI INST OF ONCOLOGY
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