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Transcription mesosome Med23 subunit serving as target for preventing or treating cancer

A subunit and gene technology, applied in the field of cancer prevention or treatment, can solve the problems of low chemotherapy efficiency, lost operation opportunities, and severe toxic and side effects

Active Publication Date: 2014-03-26
CENT FOR EXCELLENCE IN MOLECULAR CELL SCI CHINESE ACAD OF SCI
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

Lung cancer is a unique type of disease. More than 80% of patients are already in the advanced stage when they see a doctor, and they lose the chance of surgery. The efficiency of chemotherapy is low, the toxicity is large, and the 5-year survival rate is less than 15%.
[0007] At present, there is no mature tumor-targeted treatment method for Ras protein and its downstream MAP kinase signaling pathway in this field, so there is an urgent need to develop specific targets for the prevention or treatment of cancer

Method used

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  • Transcription mesosome Med23 subunit serving as target for preventing or treating cancer
  • Transcription mesosome Med23 subunit serving as target for preventing or treating cancer
  • Transcription mesosome Med23 subunit serving as target for preventing or treating cancer

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0102] Loss of Med23 slows down the growth rate of A549 cells and weakens the tumorigenic ability of A549 cells in vitro and in vivo

[0103] Experimental method: Using the expression of Med23 in retrovirus-based RNAi knockdown A549 cells (a non-small cell lung cancer cell line, which contains activating K-ras mutation), the cells of RNAi and control A549 cells were counted. The results showed that after knockdown Med23, the growth rate of A549 cells was significantly slower, indicating that Med23 was involved in the process of regulating the growth of A549 cells ( figure 1 B).

[0104] At the same time, Soft Agar Colony Formation Assay was performed on RNAi and control A549 cells, and it was found that the tumorigenic ability of A549 cells with RNAi Med23 was significantly weakened. The number and diameter of colony formed by the two were counted, and it was found that the colony formed by Knockdown cells was smaller than that of A549 cells. less, and very small and loose ( ...

Embodiment 2

[0108] Deletion of Med23 significantly reduces the efficiency of Oncogene Ras transformation into immortalized MEFs

[0109] It is known that Oncogene ras can transform immortalized MEFs in vitro, and the transformed MEFs will lose contact inhibition and be able to grow in suspension in soft agar to form clones, and eventually form tumors in nude mice subcutaneously. This example attempts to detect whether Med23 causes the above phenomenon by affecting ras.

[0110] It was found that the efficiency of Ras transforming Med23- / - MEF cells was greatly reduced compared with the wild type, and the number and size of clones formed ( figure 2 B. figure 2 C), and the subcutaneous tumorigenic ability of nude mice was significantly inferior to that of WT MEF cells ( figure 2 D), indicating that the loss of Med23 affects the process of Oncogene ras transformation.

Embodiment 3

[0112] Deletion of Med23 has no significant effect on the efficiency of Oncogene c-myc to transform immortalized MEFs

[0113] Different from ras transformation, the inventors found that the efficiency of c-myc transforming Med23- / - MEF cells was not significantly different from that of wild type, and the size and number of clones formed were similar to those of WT MEF ( image 3 C. image 3 D), indicating that the deletion of Med23 has little effect on Oncogene c-myc, thus further explaining the correlation between Med23 and Ras / MAPK signaling pathway.

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Abstract

The invention relates to a transcription mesosome Med23 subunit serving as a target for preventing or treating cancer. Specifically, the deletion of the transcription mesosome Med23 can influence the growth and tumor forming capacity of the ras-active lung cancer cell strain and obviously reduce the conversion efficiency from oncogene ras into MEF cell. Meanwhile, the expression quantity of Med23 is obviously increased in the conversion process; and the result of chip analysis shows that the deletion of Med23 influences the expression of the ras feature gene, and the Med23 acts with Elk1 to together regulate the cell cycle / cell proliferation related gene. The Med23 is remarkably highly expressed in the ras-active lung cancer cell strain and a clinical sample of lung cancer, and the expression quantity is remarkably related to prognosis; and the deletion of Med23 also can reduce the tolerance of the cancer cells to the chemotherapeutic drugs. Therefore, the Med23 is a potential cancer treatment target.

Description

technical field [0001] The invention belongs to the fields of molecular biology and biomedicine, and specifically relates to a transcription mediator Med23 subunit used as a target for preventing or treating cancer. Background technique [0002] Malignant tumor is a kind of disease that seriously threatens human health and life at present. It is a new organism formed by malignant transformation and clonal proliferation of cells with division potential after being affected by carcinogenic factors. The occurrence of tumors is often caused by genetic and environmental carcinogenic factors in the body in a sequential or coordinated manner, causing damage and mutation of genetic material DNA, accompanied by activation of multiple oncogenes and inactivation of tumor suppressor genes, resulting in continuous proliferation and transformation of normal cells. Eventually cancerous. [0003] Lung cancer has become one of the tumors with the highest morbidity and mortality in the world...

Claims

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Application Information

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IPC IPC(8): A61K45/00A61K39/395A61K38/16A61K48/00C12N5/09A61P35/00
Inventor 王纲杨旭
Owner CENT FOR EXCELLENCE IN MOLECULAR CELL SCI CHINESE ACAD OF SCI
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