Application of phenethyl caffeate in preparation of anti-cervical cancer drugs

A technology of phenethyl caffeate and cervical cancer, which is applied in the field of medicine and can solve problems such as tissue damage, drug resistance, and poor radiosensitivity

Pending Publication Date: 2022-04-22
GUIZHOU UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

Surgery, radiotherapy and chemotherapy are currently the main clinical treatment methods for cervical cancer, but both have limitations
70% of patients are diagnosed at an advanced stage and are not suitable for surgical treatment. Cervical squamous cell carcinoma is relatively sensitive to radiotherapy, but radiotherapy can easily cause damage to normal tissues around the tumor. Cervical adenocarcinoma is rela

Method used

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  • Application of phenethyl caffeate in preparation of anti-cervical cancer drugs
  • Application of phenethyl caffeate in preparation of anti-cervical cancer drugs
  • Application of phenethyl caffeate in preparation of anti-cervical cancer drugs

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0052] Experimental purpose: To illustrate the effect of CAPE on growth inhibition of 4 kinds of human cervical cancer cells through CCK-8 and clone formation experiments.

[0053] Experimental design: On human cervical cancer cell lines HeLa, MS751, SiHa and Caski, CCK-8 and clone formation experiments were used to illustrate the effect of CAPE on growth inhibition of four human cervical cancer cell lines. The result is as Figure 1-8 shown.

[0054] Analysis of results: After CAPE treatment, the viability of HeLa, MS751, SiHa and Caski cells decreased significantly.

[0055] The results showed that CAPE can inhibit the growth of cervical cancer cells.

Embodiment 2

[0057] Experimental purpose: To illustrate the effect of CAPE on apoptosis of cervical cancer cells by TUNEL and Western Blot experiments.

[0058] Experimental design: On human cervical cancer cells HeLa and SiHa, the effect of CAPE on cervical cancer cell apoptosis was determined by TUNEL and Western Blot. The result is as Figure 9-16 shown.

[0059] Analysis of the results: After CAPE treatment, the apoptosis levels of HeLa and SiHa cells were significantly increased.

[0060] The results showed that CAPE could promote the apoptosis of cervical cancer cells.

Embodiment 3

[0062] Experimental purpose: To illustrate the effect of CAPE on the interaction between E6AP and p53 through co-immunoprecipitation experiments.

[0063] experimental design:

[0064] On human cervical cancer cell lines HeLa, MS751, SiHa, Caski and HEK 293T cells, the changes in the interaction level of E6AP and p53 after CAPE treatment were determined by co-immunoprecipitation method. The result is as Figure 17-21 shown.

[0065] Analysis of results: After CAPE treatment, the level of E6AP combined with p53 was significantly reduced, and the interaction between the two was weakened.

[0066] The results indicated that CAPE could inhibit the interaction between E6AP and p53 and reduce the combination of the two.

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Abstract

The invention provides a caffeic acid phenethyl ester as a medicine for resisting cervical cancer. The invention provides application of caffeic acid phenethyl ester as an E6AP/p53 compound inhibitor and an inhibitor for ubiquitination degradation of p53. Experimental research shows that in a cell experiment, CAPE can inhibit the interaction between E6AP and p53 in an HR-HPV positive cervical cancer cell line, reduce the ubiquitination modification level of p53, prolong the half-life period of p53 and increase the level of p53.

Description

technical field [0001] The invention discloses the application of phenethyl caffeate in the preparation of anti-cervical cancer drugs, belonging to the technical field of medicine. Background technique [0002] E6-associated protein (E6-associated protein, E6AP) is a ubiquitin-activating enzyme (E3), which is highly expressed in HR-HPV positive cervical cancer. E6AP can combine with E6 to form an E6 / E6AP complex, and the two can combine with the tumor suppressor protein p53 to form an E6AP / E6 / p53 complex, which mediates the ubiquitination and degradation of p53, reduces the level of p53, and inhibits its effect on cells. Growth regulation, causing cell proliferation and malignant transformation. [0003] p53 can initiate DNA damage repair, cause cell cycle arrest, and induce cell apoptosis. The occurrence of tumors is mostly related to the mutation or deletion of p53. In most cervical cancer cell lines, p53 is wild type and has biological functions, but its tumor suppresso...

Claims

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Application Information

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IPC IPC(8): A61K31/216A61P35/00
CPCA61K31/216A61P35/00
Inventor 王呈呈李威石忠秀黄勇龙青青程志颖
Owner GUIZHOU UNIV
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