CN114377001A - Application of caffeic acid phenethyl ester in preparation of anti-cervical cancer drugs - Google Patents
Application of caffeic acid phenethyl ester in preparation of anti-cervical cancer drugs Download PDFInfo
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- CN114377001A CN114377001A CN202210193752.9A CN202210193752A CN114377001A CN 114377001 A CN114377001 A CN 114377001A CN 202210193752 A CN202210193752 A CN 202210193752A CN 114377001 A CN114377001 A CN 114377001A
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- WWVKQTNONPWVEL-UHFFFAOYSA-N caffeic acid phenethyl ester Natural products C1=C(O)C(O)=CC=C1C=CC(=O)OCC1=CC=CC=C1 WWVKQTNONPWVEL-UHFFFAOYSA-N 0.000 title claims abstract description 74
- SWUARLUWKZWEBQ-UHFFFAOYSA-N phenylethyl ester of caffeic acid Natural products C1=C(O)C(O)=CC=C1C=CC(=O)OCCC1=CC=CC=C1 SWUARLUWKZWEBQ-UHFFFAOYSA-N 0.000 title claims abstract description 74
- SWUARLUWKZWEBQ-VQHVLOKHSA-N phenethyl caffeate Chemical compound C1=C(O)C(O)=CC=C1\C=C\C(=O)OCCC1=CC=CC=C1 SWUARLUWKZWEBQ-VQHVLOKHSA-N 0.000 title claims abstract description 73
- 206010008342 Cervix carcinoma Diseases 0.000 title claims abstract description 35
- 208000006105 Uterine Cervical Neoplasms Diseases 0.000 title claims abstract description 35
- 201000010881 cervical cancer Diseases 0.000 title claims abstract description 35
- 239000003560 cancer drug Substances 0.000 title description 2
- 101100155061 Homo sapiens UBE3A gene Proteins 0.000 claims abstract description 21
- 101100155062 Mus musculus Ube3a gene Proteins 0.000 claims abstract description 21
- 102100030434 Ubiquitin-protein ligase E3A Human genes 0.000 claims abstract description 21
- 230000034512 ubiquitination Effects 0.000 claims abstract description 18
- 238000010798 ubiquitination Methods 0.000 claims abstract description 18
- 230000015556 catabolic process Effects 0.000 claims abstract description 14
- 238000006731 degradation reaction Methods 0.000 claims abstract description 14
- 239000003112 inhibitor Substances 0.000 claims abstract description 7
- 239000003814 drug Substances 0.000 claims abstract description 5
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- 238000001727 in vivo Methods 0.000 description 3
- 102000004169 proteins and genes Human genes 0.000 description 3
- 108090000623 proteins and genes Proteins 0.000 description 3
- 108090000397 Caspase 3 Proteins 0.000 description 2
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- 102100026548 Caspase-8 Human genes 0.000 description 2
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- 102100026550 Caspase-9 Human genes 0.000 description 2
- 108090000566 Caspase-9 Proteins 0.000 description 2
- 229920000776 Poly(Adenosine diphosphate-ribose) polymerase Polymers 0.000 description 2
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- IZTQOLKUZKXIRV-YRVFCXMDSA-N sincalide Chemical compound C([C@@H](C(=O)N[C@@H](CCSC)C(=O)NCC(=O)N[C@@H](CC=1C2=CC=CC=C2NC=1)C(=O)N[C@@H](CCSC)C(=O)N[C@@H](CC(O)=O)C(=O)N[C@@H](CC=1C=CC=CC=1)C(N)=O)NC(=O)[C@@H](N)CC(O)=O)C1=CC=C(OS(O)(=O)=O)C=C1 IZTQOLKUZKXIRV-YRVFCXMDSA-N 0.000 description 2
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- 241000241413 Propolis Species 0.000 description 1
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- 239000004480 active ingredient Substances 0.000 description 1
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- 239000003963 antioxidant agent Substances 0.000 description 1
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- 229940069949 propolis Drugs 0.000 description 1
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- 231100000331 toxic Toxicity 0.000 description 1
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- QAIPRVGONGVQAS-DUXPYHPUSA-N trans-caffeic acid Chemical class OC(=O)\C=C\C1=CC=C(O)C(O)=C1 QAIPRVGONGVQAS-DUXPYHPUSA-N 0.000 description 1
- 230000005748 tumor development Effects 0.000 description 1
Images
Classifications
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K31/00—Medicinal preparations containing organic active ingredients
- A61K31/21—Esters, e.g. nitroglycerine, selenocyanates
- A61K31/215—Esters, e.g. nitroglycerine, selenocyanates of carboxylic acids
- A61K31/216—Esters, e.g. nitroglycerine, selenocyanates of carboxylic acids of acids having aromatic rings, e.g. benactizyne, clofibrate
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P35/00—Antineoplastic agents
Abstract
The invention provides caffeic acid phenethyl ester serving as a medicine for resisting cervical cancer. The invention provides caffeic acid phenethyl ester which is applied as an E6AP/p53 compound inhibitor and an inhibitor of p53 ubiquitination degradation. Experimental research shows that CAPE can inhibit the interaction between E6AP and p53 in HR-HPV positive cervical cancer cell lines, reduce the ubiquitination modification level of p53, prolong the half-life of p53 and raise the p53 level.
Description
Technical Field
The invention discloses application of caffeic acid phenethyl ester in preparation of an anti-cervical cancer medicament, and belongs to the technical field of medicines.
Background
The E6 related protein (E6-associated protein, E6AP) is ubiquitin-activating enzyme (E3) and has high expression in HR-HPV positive cervical carcinoma. E6AP can be combined with E6 to form an E6/E6AP complex, and the two can be combined with oncostatin p53 to form an E6AP/E6/p53 complex, mediate ubiquitination degradation of p53, reduce the level of p53, inhibit the regulation effect of the p53 on cell growth, and cause cell unlimited proliferation and malignant transformation.
p53 initiates DNA damage repair, causes cell cycle arrest, induces apoptosis, and tumor development is mostly related to mutation or deletion of p 53. In most of cervical cancer cell lines, p53 is wild type and has biological functions, but its half-life is short and its expression level is low, so that its cancer-suppressing function is limited. Ubiquitination modification is an important means of regulating the level of p53 in cells. In HR-HPV infected cervical carcinoma, E6AP mediated ubiquitination degradation is the major pathway of p53 degradation.
HR-HPV positive people account for a high proportion of cervical cancer patients, the incidence rate of cervical cancer gradually increases in recent years, and the average age of the patients is remarkably reduced. Surgery and radiotherapy and chemotherapy are the main clinical methods for treating cervical cancer at present, but both have limitations. 70% of patients are diagnosed at the late stage and are not suitable for surgical treatment; cervical squamous carcinoma is relatively sensitive to radiotherapy, but the radiotherapy easily causes damage to normal tissues around the tumor; the sensitivity of the cervical adenocarcinoma to radiotherapy is relatively poor, chemotherapy is mostly adopted, however, drug resistance is easy to occur, and the chemotherapy drug has poor targeting property and strong toxic and side effects.
Therefore, a potent inhibitor of ubiquitination degradation of p53 has been sought, which promotes intracellular accumulation of p53 and exerts its cancer-suppressing function sufficiently, and which is of great significance for the treatment of diseases such as cervical cancer.
Caffeic Acid Phenethyl Ester (CAPE) is one of the main active ingredients of propolis, is Caffeic acid derivative, and has antitumor, antibacterial, and antibacterial effects,
Antioxidant, liver protecting, and ischemia-reperfusion injury resisting biological activities. The applications of inhibiting the interaction between E6AP and p53, reducing p53 ubiquitination modification, increasing the protein level of p53 and playing a role in resisting cervical cancer and the like are not reported in documents.
Disclosure of Invention
The invention aims to provide Caffeic Acid Phenethyl Ester (CAPE) serving as a medicine for resisting cervical cancer.
The invention provides caffeic acid phenethyl ester which is applied as an E6AP/p53 compound inhibitor and an inhibitor of p53 ubiquitination degradation.
Experimental research shows that CAPE can inhibit the interaction between E6AP and p53 in HR-HPV positive cervical cancer cell lines, reduce the ubiquitination modification level of p53, prolong the half-life of p53 and raise the p53 level.
The above cells are specifically human cervical cancer cells.
The invention also comprises the application of the caffeic acid phenethyl ester in preparing products, and the application of the products comprises the following steps:
1. inhibiting the growth of cervical cancer cells.
2. Promoting the cervical cancer cell to generate apoptosis.
The inventor of the invention finds that CAPE can effectively inhibit the combination of E6AP and p53 protein in HR-HPV positive cervical cancer cell lines, so that the concentration of the in vivo tumor suppressor protein p53 protein is increased, and then the formation or growth of HR-HPV positive cervical cancer cells can be effectively inhibited by accumulating more p53 protein in vivo, and finally the purpose of inhibiting cancer is realized.
The inventor of the invention finds that CAPE can effectively inhibit the ubiquitination level of p53 protein, can also improve the concentration of oncoprotein p53 protein to be improved, and then can effectively inhibit the formation or growth of HR-HPV positive cervical cancer cells by accumulating more p53 protein in vivo, thereby finally realizing the purpose of inhibiting cancer.
The invention has important significance for treating cervical cancer.
Drawings
FIG. 1 shows the change of growth of HeLa cells after CAPE treatment;
FIG. 2 shows the change in growth of cells after CAPE treatment of MS751 cells;
FIG. 3 shows the change in cell growth after CAPE treatment of SiHa cells;
FIG. 4 shows the change in growth of Caski cells after CAPE treatment;
FIG. 5 shows the change of growth of cell clones after the HeLa cells were treated with CAPE;
FIG. 6 shows the change in growth of clones of MS751 cells after CAPE treatment;
FIG. 7 shows the change in clonal growth of SiHa cells after CAPE treatment;
FIG. 8 shows the change in clonal growth of Caski cells after CAPE treatment;
FIG. 9 shows the change of apoptosis of HeLa cells treated with CAPE;
FIG. 10 shows the change in apoptosis of SiHa cells after CAPE treatment;
FIG. 11 is a statistical plot of apoptosis of HeLa and SiHa cells treated with CAPE;
FIG. 12 shows the change in the expression levels of apoptosis-related proteins PARP, Caspase-8 and Bax after the treatment of HeLa cells with CAPE;
FIG. 13 shows the change in the levels of apoptosis-related proteins Caspase-3, Caspase-9 and Bcl-2 after CAPE treatment of HeLa cells;
FIG. 14 shows the change in the expression levels of apoptosis-related proteins PARP, Caspase-8 and Bax in SiHa cells treated with CAPE;
FIG. 15 is a graph showing the change in the levels of apoptosis-related proteins Caspase-3, Caspase-9 and Bcl-2 following CAPE treatment of SiHa cells;
FIG. 16 is a statistical graph of the change in the ratios of apoptosis-related proteins Bax and Bcl-2 after CAPE treatment of HeLa and SiHa cells;
FIG. 17 is the change in interaction of E6AP with p53 protein after treatment of HeLa cells with CAPE;
FIG. 18 shows the change in interaction of E6AP with p53 protein after CAPE treatment of MS751 cells;
FIG. 19 is the change in interaction of E6AP with p53 protein after SiHa cells were treated with CAPE;
FIG. 20 is the change in the interaction of E6AP with p53 protein after CAPE treatment of Caski cells;
FIG. 21 is the change in interaction of E6AP with p53 protein following CAPE treatment of HEK 293T cells;
FIG. 22 is the change in the ubiquitination level of p53 after CAPE treatment of HeLa cells;
FIG. 23 is the change in the ubiquitination level of p53 following CAPE treatment of MS751 cells;
FIG. 24 is the change in the level of ubiquitination of p53 following CAPE treatment of HEK 293T cells;
FIG. 25 is the change in the degradation rate of p53 after CAPE treatment of HeLa cells;
FIG. 26 shows the change in degradation rate of p53 after CAPE treatment of MS751 cells;
FIG. 27 is the change in the degradation rate of p53 after CAPE treatment of SiHa cells;
FIG. 28 is the change in the degradation rate of p53 in Caski cells treated with CAPE;
FIG. 29 shows the change in the expression level of p53 protein in HeLa cells treated with CAPE.
FIG. 30 shows the change in the expression level of p53 protein in MS751 cells treated with CAPE.
FIG. 31 shows the change in the expression level of p53 protein in SiHa cells treated with CAPE.
FIG. 32 shows the change in the expression level of p53 protein in Caski cells treated with CAPE.
Detailed Description
The invention is further described below with reference to the accompanying drawings. The following examples are only for illustrating the technical solutions of the present invention more clearly, and the protection scope of the present invention is not limited thereby.
Example one
Purpose of the experiment: the effect of CAPE on the growth inhibition of 4 human cervical cancer cells was demonstrated by CCK-8 and clonogenic experiments.
Experiment design: the effect of CAPE on the growth inhibition of 4 human cervical cancer cells was demonstrated by CCK-8 and clonogenic experiments on the human cervical cancer cell lines HeLa, MS751, SiHa and Caski. The results are shown in FIGS. 1 to 8.
And (4) analyzing results: survival of HeLa, MS751, SiHa and Caski cells was significantly reduced when treated with CAPE.
The results indicate that CAPE inhibits the growth of cervical cancer cells.
Example two
Purpose of the experiment: the effect of CAPE on apoptosis of cervical cancer cells was demonstrated by TUNEL and Western Blot experiments.
Experiment design: the effect of CAPE on apoptosis of cervical cancer cells was determined by TUNEL and Western Blot on human cervical cancer cells HeLa, SiHa. The results are shown in FIGS. 9-16.
And (4) analyzing results: when CAPE treatment was given, the level of apoptosis in HeLa and SiHa cells was significantly increased.
The results indicate that CAPE promotes apoptosis in cervical cancer cells.
EXAMPLE III
Purpose of the experiment: the effect of CAPE on the interaction of E6AP and p53 was demonstrated by co-immunopropractition experiments.
Experiment design:
changes in the level of E6AP interaction with p53 following CAPE treatment were determined by co-immunopropractitation on the human cervical cancer cell lines HeLa, MS751, SiHa, Caski and HEK 293T cells. The results are shown in FIGS. 17-21.
And (4) analyzing results: when CAPE treatment was given, the level of E6AP bound to p53 was significantly reduced and the interaction between the two was reduced.
The results indicate that CAPE can inhibit the interaction of E6AP with p53, and reduce the binding of the two.
Example four
Purpose of the experiment: the effect of CAPE on the ubiquitination level of p53 protein was demonstrated by Western Blot experiments.
Experiment design: the effect of CAPE on the ubiquitination level of p53 was demonstrated by Western Blot experiments on the human cervical cancer cell lines HeLa, MS751 and HEK 293T. The results are shown in FIGS. 22-24.
And (4) analyzing results: HeLa, MS751 and HEK-293T cells were treated with CAPE and the level of p53 ubiquitination was reduced.
The results show that: CAPE can inhibit ubiquitination levels of p 53.
EXAMPLE five
Purpose of the experiment: the influence of CAPE on the degradation rate of p53 protein was demonstrated by Western Blot experiment.
Experiment design: the influence of CAPE on the degradation rate of p53 protein was determined by Western Blot method on human cervical cancer cells HeLa, MS751, SiHa, Caski. The results are shown in FIGS. 25-28.
And (4) analyzing results: the rate of p53 protein degradation decreased significantly when CAPE was administered.
The results indicate that CAPE can inhibit the degradation of p53 protein.
EXAMPLE six
Purpose of the experiment: the effect of CAPE on the expression level of p53 protein was demonstrated by Western Blot experiment.
Experiment design: the influence of CAPE on the expression level of p53 protein was demonstrated by Western Blot experiments on human cervical cancer cell lines HeLa, MS751, SiHa and Caski. The results are shown in FIGS. 29-32.
And (4) analyzing results: when CAPE was administered, the expression level of p53 protein was significantly increased. The results show that: CAPE can up-regulate the expression level of p53 protein.
The above description is only a preferred embodiment of the present invention, and it should be noted that, for those skilled in the art, several modifications and variations can be made without departing from the technical principle of the present invention, and these modifications and variations should also be regarded as the protection scope of the present invention.
Claims (4)
1. Application of caffeic acid phenethyl ester in preparing anti-cervical cancer medicine is provided.
2. The use according to claim 1, wherein the cervical cancer is HR-HPV positive cervical cancer.
3. Application of caffeic acid phenethyl ester in preparing E6AP/p53 compound inhibitor is provided.
4. Application of caffeic acid phenethyl ester in preparing inhibitor for ubiquitination degradation of p 53.
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| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN202210193752.9A CN114377001A (en) | 2022-03-01 | 2022-03-01 | Application of caffeic acid phenethyl ester in preparation of anti-cervical cancer drugs |
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| Application Number | Priority Date | Filing Date | Title |
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| CN202210193752.9A CN114377001A (en) | 2022-03-01 | 2022-03-01 | Application of caffeic acid phenethyl ester in preparation of anti-cervical cancer drugs |
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| CN202210193752.9A Pending CN114377001A (en) | 2022-03-01 | 2022-03-01 | Application of caffeic acid phenethyl ester in preparation of anti-cervical cancer drugs |
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Cited By (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN115819432A (en) * | 2022-11-16 | 2023-03-21 | 成都市华大基因医学研究院有限公司 | Compound and medicine for treating cervical cancer |
Citations (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN104592182A (en) * | 2014-12-31 | 2015-05-06 | 中山大学 | Caffeic acid phenethyl ester compounds and preparation method and application thereof |
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2022
- 2022-03-01 CN CN202210193752.9A patent/CN114377001A/en active Pending
Patent Citations (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN104592182A (en) * | 2014-12-31 | 2015-05-06 | 中山大学 | Caffeic acid phenethyl ester compounds and preparation method and application thereof |
Non-Patent Citations (2)
| Title |
|---|
| Y.-J. LEE ET AL.: "Involvement of tumor suppressor protein p53 and p38 MAPK in caffeic acid phenethyl ester-induced apoptosis of C6 glioma cells" * |
| 王月华;常化松;尹旭升;刘新迎;玄红专;: "白杨素与咖啡酸苯乙酯抗肿瘤活性比较" * |
Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN115819432A (en) * | 2022-11-16 | 2023-03-21 | 成都市华大基因医学研究院有限公司 | Compound and medicine for treating cervical cancer |
| CN115819432B (en) * | 2022-11-16 | 2024-02-23 | 成都市华大基因医学研究院有限公司 | Compound and medicine for treating cervical cancer |
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Application publication date: 20220422 |