CN107496417A - Epigallo-catechin gallate (EGCG) prepares the application of targeted drug - Google Patents
Epigallo-catechin gallate (EGCG) prepares the application of targeted drug Download PDFInfo
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Abstract
The present invention provides a kind of application of Epigallo-catechin gallate (EGCG) in the medicines of targeted inhibition ERs ER α 36 are prepared.The present invention verifies that Epigallo-catechin gallate (EGCG) (EGCG) can significantly inhibit the propagation of the high expression tumour cells of ER α 36, cause phase cell cycle G1 to be blocked through biological experiment, suppresses cell migration, invasive ability, apoptosis-induced generation.Target spot effect is clear and definite, especially obvious to the inhibition of the tumour cell of ER α 36 unconventionality expression.A kind of 36 selectively targeted inhibitor of ER α can be used as to due to the unconventionality expression cells play inhibitory action of ER α 36.The present invention provides a kind of new active drug for the development of clinical 36 abnormal personalized treatments of targeting ER α.
Description
Technical field
The invention belongs to biomedicine field, is related to Epigallo-catechin gallate (EGCG) (Epigallocatechin
Gallate, EGCG) application in the medicines of targeted inhibition ERs ER- α 36 are prepared.
Background technology
ERs is a kind of important receptor protein, has in wide variety of different types of cells and expresses and play
Corresponding effect.In classical estrogen shaping modes, estrogen by with ERs (estrogen receptor,
ER) combine, change receptor conformation and gone to as transcription factor in karyon, direct regulation and control expression of target gene, this mechanism is referred to as
The estrogen receptor conduction that core starts (i.e. genome is adjusted).The ERs that estrogen can also position with plasma membrane is combined,
The cascade reaction of downstream signaling pathway is activated so as to the expression of some genes of indirect adjustments and controls, this mechanism quilt by protein phosphorylation
The estrogen receptor conduction that referred to as film starts (i.e. non genome is adjusted).Compared with female hormone receptor gene group regulates and controls, non-genomic
Group regulation can regulate and control more polygenes, participate in cell propagation, survival, apoptosis and differentiation.
ERs has ER- α and ER- β two types, and ER- α have ER- α 66, ER- α 46 and 36 3 kinds of hypotypes of ER- α again.
ER- α 66 have similar protein structure with ER- β, are all made up of the functional domain of 3 independences but interaction：A/B
Area is transcriptional activation domain (including AF-1 and AF-2), and C areas are DNA binding domain, and D/E/F areas are ligand binding domains, main
It is distributed in nucleus and endochylema, the estrogen receptor pathway that mediation core starts.
ER- α 36 are that the molecular weight cloned and found in 2005 is a kind of 36kD estrogen receptor alpha hypotype.With ER- α 66
Compare, ER- α 36 lack 2 transcription activating domains (AF-1 and AF-2), but still retain DNA binding domain and part it is Dimerized and
Ligand binding domains, it is primarily targeted for cell membrane (50%) and endochylema (40%).The part scopes of ER- α 36 are more extensive, can quilt
E2 α, E2 β, E3, E4 activation, mediate quick non genome signal transduction pathway by membrane estrogen receptor, activate downstream MEK1/2
With ERK1/2 signal paths, various biological effects are produced, the differentiation, propagation with cell have substantial connection.
Expression of the ER- α 36 under a variety of pathological states such as malignant tumour has obvious abnormal elevated phenomenon.Stomach signet ring
Expression in cell carcinoma tumor tissue is apparently higher than normal structure.In triple negative breast cancer, the ER- α 36 of height expression can not be by
Antiestrogen TAM suppresses, so that tumor drug resistance.ER- α 36 are also expressed in adenocarcinoma of lung, clear-cell carcinoma in high,
It is related to late period metastases in local lymph node, it is negatively correlated with Overall survival and DFS phase.In normal liver tissue, ER- α 36
Expression is negative, but in liver cancer tissue, overexpression is but presented in ER- α 36, and the generation and progress that this may be to liver cancer are related.
It has also been found that the expression of ER- α 36 is related to lymphatic metastasis in Human Laryngeal Cancer Cell and patient specimen.Estrogen action is after ER- α 36
Angiogenesis and transfer factor expression are raised, the enhancing of laryngeal cancer cell resistance ability.
In summary, targeted therapy is carried out for the related abnormal cell proliferation diseases of all kinds of ER- α 36, had important
Clinical meaning.EGCG is a kind of water-soluble components extracted from green tea, is content highest component in catechin, has research aobvious
Show that it has many-sided effect such as antibacterial, antiviral, anti-oxidant, antiangiogenic, anti-inflammatory, but definite mechanism of action is still endless
All clear Chu.
The content of the invention
It is an object of the invention to provide a kind of Epigallo-catechin gallate (EGCG) prepare targeted inhibition estrogen by
Application in the medicines of body ER- α 36.The present invention is to provide a kind of new targeted inhibition ERs ER- α 36 antineoplastic
Thing, it can specifically be combined with ERs ER- α 36 and suppress its activity, research shows that epigallocatechin is not eaten
Sub- acid esters (EGCG) is connected by hydrogen bond with ER- α 36 Lys79, Arg87, Lys130, Asn131, realizes antitumor purpose.
EGCG structural formulas are as follows：
Epigallo-catechin gallate (EGCG) (EGCG) can be by specifically targetting with reference to ER- α 36, and then suppresses it
Activity, so as to significantly inhibit the propagation of the high expression stomach signet ring cell cancer cells of ER- α 36, cause phase cell cycle G1 to be blocked, suppress
Cell migration, invasive ability, apoptosis-induced generation.Epigallo-catechin gallate (EGCG) EGCG provided by the invention can also press down
The high expression breast cancer cells of ER- α 36 processed.Epigallo-catechin gallate (EGCG) (EGCG) is acted on referring to Fig. 1 with ER- α 36.
The present invention compared with the existing technology has advantages below and effect：
More lack currently for the medicine of the disease caused by ER- α 36 unconventionality expression, and epigallocatechin gallate
Catechin gallate EGCG simultaneously fails to understand as a kind of multi-functional compound naturally extracted, its target molecule to play a role
Really.Therefore, the present invention finds 36 selectively targeted inhibitor of ER- α by correlative study, specify that epigallocatechin does not have
Infanticide acid esters (Epigallocatechin Gallate, EGCG) by selectively targeted combination and can suppress ERs
ER- α 36 function, action target spot is clear and definite, especially obvious to the inhibition of the tumour cell of ER- α 36 unconventionality expression：Table does not have
After infanticide catechin and gallate EGCG is by selectively targeted ERs ER- α 36, it can substantially suppress 36 high tables of ER- α
Tumor cell proliferation, migration, the invasive ability reached, inducing cell apoptosis occur.A kind of ER- α 36 can be used as selectively targeted
Inhibitor is to due to the unconventionality expression cells play inhibitory action of ER- α 36.The present invention is clinical 36 abnormal personalizations of targeting ER- α
The development for the treatment of provides a kind of new active drug.
Brief description of the drawings
Fig. 1 is the medicine EGCG that targeting ER- α 36 are predicted by molecular docking software MOE
Ester EGCG, pass through hydrogen bond and ER- α 36 Lys79, Arg87, Lys130, the schematic diagram of Asn131 connections.
It is thin that Fig. 2 is that Epigallo-catechin gallate (EGCG) EGCG can significantly inhibit the high expression stomach signet ring cell cancer of ER- α 36
Born of the same parents breed.
Fig. 3 is that Epigallo-catechin gallate (EGCG) EGCG can significantly inhibit the high expression breast cancer cell increasings of ER- α 36
Grow.
Fig. 4 is that scratch experiment proves that Epigallo-catechin gallate (EGCG) EGCG can significantly inhibit the high expression stomaches of ER- α 36
Signet ring cell cancer cell GCSR-1-6 transfer abilities.
Fig. 5 proves that Epigallo-catechin gallate (EGCG) EGCG can significantly inhibit the high expression stomaches of ER- α 36 to wear film experiment
Signet ring cell cancer cell GCSR-1-6 transfer abilities.
It is thin that Fig. 6 is that Epigallo-catechin gallate (EGCG) EGCG can significantly inhibit the high expression stomach signet ring cell cancer of ER- α 36
Born of the same parents' GCSR-1-6 invasive abilities.
Fig. 7 A and Fig. 7 B are that Epigallo-catechin gallate (EGCG) EGCG acts on the high expression stomach signet ring cells of ER- α 36
Generation G1 phases cell cycle block after cancer cell GCSR-1-6.
Fig. 8 is that Epigallo-catechin gallate (EGCG) EGCG acts on the high expression stomach signet ring cell cancer cells of ER- α 36
Proliferation-associated protein expression changes after GCSR-1-6.
Fig. 9 is that Epigallo-catechin gallate (EGCG) EGCG suppresses the high expression stomach signet ring cell cancer cells of ER- α 36
GCSR-1-6 downstreams PI3K/Akt, MAPK/ERK signal path.
Figure 10 is that Epigallo-catechin gallate (EGCG) EGCG acts on the high expression stomach signet ring cell cancer cells of ER- α 36
After GCSR-1-6, reactive oxygen species (Reactive Oxygen Species, ROS) increase.
Figure 11 is that Epigallo-catechin gallate (EGCG) EGCG acts on the high expression stomach signet ring cell cancer cells of ER- α 36
Apoptosis flow cytometer detection figure after GCSR-1-6.
Figure 12 is that Epigallo-catechin gallate (EGCG) EGCG acts on the high expression stomach signet ring cell cancer cells of ER- α 36
Apoptosis result column analysis chart after GCSR-1-6.
Figure 13 Epigallo-catechin gallate (EGCG)s EGCG acts on the high expression stomach signet ring cell cancer cells of ER- α 36
After GCSR-1-6, apoptosis-related protein expression changes.
Embodiment
The present invention is described further with reference to the drawings and specific embodiments.These embodiments are merely to illustrate, but are not limited
The present invention.
Embodiment 1：The targeted drugs of ER- α 36 screen in MPD3 medicinal plant databases
2295 kinds of phytochemicals are included in MPD3 medicinal plant databases, forecasting software MOE is docked by protein ligand
V2014.0901,2.4GHz operating systems, under the conditions of 8GB RAM (x86) operating platform, according to molecule
S scorings are docked, screening may target ER- α 36 phytochemicals.According to the selection result, 6 medicines enter before we choose ranking
Row subsequent analysis, it is flavonoid class material, is shown in Table 1.
Table 1：MOE protein ligands docking software screening method, which obtains 6 kinds, may target the phytochemicals of ER- α 36
We further utilize Molinspiration softwares, assess the lipid of the 6 kinds of materials filtered out, divide
Sub- amount, hydrogen bond donor quantity, hydrogen bond receptor quantity, the quantity of rotatable key, carry out pharmacokinetics prediction and evaluation.According to
" Lipinski five rule ", in 6 kinds of phytochemicals Epigallo-catechin gallate (EGCG) EGCG lipids more preferably,
Violation item number is less, possesses preferably absorption and permeance property, is shown in Table 2.
Table 2：Molinspiration software configurations feature scores
We also 6 kinds of prediction medicines are carried out using Molinspiration softwares GPCR parts, ion channel modulators,
The prediction scoring of the bioactivity such as nuclear receptor ligands, kinase inhibitor, protease inhibitors.Judgment criteria is：Scoring>0, possess life
Thing activity；-5<Prediction scoring<0, medium activity；Prediction scoring<- 5, without bioactivity.Epigallocatechin nutgall
Acid esters EGCG scorings in the prediction of above-mentioned bioactivity are positive number, show may possess above-mentioned biological activity, can be used as ER-
The targeted drug optimal selections of α 36, subsequent experimental analysis is carried out, is shown in Table 3.
Table 3：Bioactivity prediction scoring
Embodiment 2：The high expression stomach signet ring cell cancers of Epigallo-catechin gallate (EGCG) EGCG targeted inhibition ER- α 36
Cell is bred
Choose stomach signet ring cell cancer cell (the high expression GCSR-1-6 of ER- α 36, the 36 low tables of ER- α of the differential expressions of ER- α 36
Up to GCSR-1-11), for evaluating Epigallo-catechin gallate (EGCG) EGCG to the differential expression stomach signet ring cell cancers of ER- α 36
The influence of cell growth inhibition.Exponential phase cell is chosen, 96 orifice plate cell-seeding-densities are 3000/ hole, 37 DEG C, 5%
CO2, after 10%FBS-RPMI1640 kind plate cultures 16h, add prepared by 10%FBS-RPMI1640 respective concentration EGCG (0,
6.25,12.5,25,50,100 μ g/ml) processing cell.After 72h, after 10%CCK-8 is incubated 1h, Bio-Rad iMarkTMEnzyme mark
Instrument detects OD490nm absorbances, calculates IC50.As a result show, Epigallo-catechin gallate (EGCG) EGCG can dose-dependant
Type suppresses cell propagation, but in the high expression stomach signet ring cell cancer cell GCSR-1-6 of ER- α 36, its half-inhibition concentration is lower,
Inhibition more preferably, is embodied clearly due to the Cytostatic to tumor cell effect for target with reference to and suppressing ER- α 36 and play
Fruit, as shown in Figure 2.
Embodiment 3：Epigallo-catechin gallate (EGCG) EGCG targeted inhibition ER- α 36 are high, and expression breast cancer cell increases
Grow
Choose breast cancer cell (the high expression MDA-MB-231 of ER- α 36, the low expressions of ER- α 36 of the differential expressions of ER- α 36
MCF-7), the differential expression breast cancer cell growths of ER- α 36 are suppressed for evaluating Epigallo-catechin gallate (EGCG) EGCG
Influence, concrete operation step is as described in Example 2.As a result show, Epigallo-catechin gallate (EGCG) EGCG can agent
Measure dependent form and suppress cell propagation, but in the high expression breast cancer cell MDA-MB-231 of ER- α 36, its half-inhibition concentration is more
Low, inhibition more preferably, is embodied clearly due to the Cytostatic to tumor cell for target with reference to and suppressing ER- α 36 and play
Effect, as shown in Figure 3.
Embodiment 4：Epigallo-catechin gallate (EGCG) EGCG suppresses the cut healing ER- of the high expressing cells of ER- α 36
The stomach signet ring cell cancer cell GCSR-1-6 of the high expression of α 36, by 1*105/ hole cell number is inoculated in six orifice plates, treats cell density
At 90% or so, three vertical lines are longitudinally marked in the middle section of cell growth with 10 μ l pipette tips.After PBS is washed three times, take pictures
Record is set to 0h.Respective concentration EGCG (the 0,3.125,6.25,12.5,25 μ g/ that addition is prepared by 10%FBS-RPMI1640
Ml cell) is handled, central cut area cell migration situation is photographed to record per 12h, amounts to 48h.As a result show, drawn after EGCG processing
Trace peak width increases compared with control group, i.e. EGCG can substantially suppress GCSR-1-6 cell migration abilities, as shown in Figure 4.
Embodiment 5：The high expressing cells of Epigallo-catechin gallate (EGCG) EGCG suppression ER- α 36 wear film ability
After the clear 16h of stomach signet ring cell cancer cell GCSR-1-6 ischemics of the high expression of ER- α 36, digestion counts.Added per hole
The cell suspension that 500 μ l RPMI-1640 or respective concentration EGCG (0,6.25,12.5,25 μ g/ml) are prepared, cell number 5*
104Individual/hole, is inoculated in upper chamber.Lower room adds 500 μ l 10%FBS-RPMI-1640 culture mediums per hole.37 DEG C, 5%CO2Culture
After 48h, cell is taken out, the cell of upper chamber is removed with cotton swab.Cell is placed in room temperature in 10% formalin and fixes 20 minutes.
PBS is rinsed three times, 5 minutes every time.0.5% violet staining 20 minutes, ddH2Rinsed 2-3 times in O.20 times of object lens of microscope regard
Upper and lower, left and right and middle five visuals field are taken to count counting of taking pictures under open country.As a result show, high concentration EGCG (25 μ g/ml) processing
After cell, wear film ability and decline about 6 times, as shown in Figure 5.
Embodiment 6：Epigallo-catechin gallate (EGCG) EGCG suppresses the high expressing cell invasive abilities of ER- α 36
Wear film cell 70 μ l 1 of paving in advance:The matrigel of 5 ratio serum-free RPMI-1640 dilutions, coagulates in 37 DEG C of incubators
Gu 60 minutes.After the clear 16h of stomach signet ring cell cancer cell GCSR-1-6 ischemics of the high expression of ER- α 36, digestion counts.Added per hole
The cell suspension that 500 μ l RPMI-1640 or respective concentration EGCG (0,6.25,12.5,25 μ g/ml) are prepared, cell number 5*
104Individual/hole, is inoculated in upper chamber.Lower room adds 500 μ l 10%FBS-RPMI-1640 culture mediums per hole.37 DEG C, 5%CO2Culture
After 72h, cell is taken out, cell mesostroma glue is sucked, the cell of upper chamber is removed with cotton swab.Cell is placed in 10% formalin
Room temperature fixes 20 minutes.PBS is rinsed three times, 5 minutes every time.0.5% violet staining 20 minutes, ddH2Rinsed 2-3 times in O.
Microscope 20 times of object lens visuals field Xia Qu upper and lower, left and right and middle five visuals field count counting of taking pictures.As a result show, high concentration
After EGCG (25 μ g/ml) processing cells, invasive ability declines about 3 times, as shown in Figure 6.
Embodiment 7：The cell cycle of the high expressing cells of Epigallo-catechin gallate (EGCG) EGCG retardance ER- α 36
The stomach signet ring cell cancer cell GCSR-1-6 of the high expression of ER- α 36 presses 1*105/ hole cell number is inoculated in six orifice plates,
After the clear 16h of ischemic, after adding respective concentration EGCG (0,12.5,25,50 μ g/ml) processing cells 36h, cell is collected, ice PBS is washed
2 times, 75% -20 DEG C of ethanol fixation is overnight.On the detection same day, fixed cell is taken out, ice PBS is washed 2 times, adds 400 μ l BD
Cell is resuspended in Pharmingen PI/RNase staining Buffer, machine testing in streaming after lucifuge is incubated at room temperature 15 minutes.
As a result show, EGCG processing after G1 phase cells dramatically increase, S phase cells substantially reduce, and cell is arrested in the G1 phases, see Fig. 7 A and
Shown in Fig. 7 B.
Embodiment 8：Epigallo-catechin gallate (EGCG) EGCG influences the GAP-associated protein GAP table of the high expressing cells of ER- α 36
Reach
The stomach signet ring cell cancer cell GCSR-1-6 of the high expression of ER- α 36 adds respective concentration EGCG (0,12.5,25,50 μ
G/ml after) handling cell 48h, cell is collected, ice PBS is washed twice.On ice RIPA lysates cracking 1h, 4 DEG C, 12000x g from
Heart 20min, collect supernatant.Bio-Rad DC kits carry out determination of protein concentration, and applied sample amount is 30 μ g/ holes, and high temperature albumen becomes
Property, PAGE gel electrophoretic separation, PVDF transferring films.10% skim milk or 5%BSA closings, primary antibody are incubated overnight, and 0.1%
TBST is washed 5 times, each 5min, and secondary antibody is incubated at room temperature 1h, and 0.1%TBST is washed 5 times, each 5min, utilizes Millipore ECL
Chemiluminescent HRP substrate kits, in Bio-Rad ChemiDocTMBar is carried out under MP chemical imaging instrument
Band detection.As a result show, cell multiple fission GAP-associated protein GAP PCNA, CDC-42 expression is lowered, stem cell factor acceptor egg
White c-Kit up-regulated expressions, cell adhesion spot kinases FAK expression are lowered, as shown in Figure 8.
PI3K/Akt, MAPK/ERK signal path molecule are lowered, as shown in Figure 9.
Protein activation shearing occurs for apoptosis-related protein PARP, caspase-3, and anti-apoptotic proteins Bcl-2 expression is lowered, from
Biting GAP-associated protein GAP LC3 expression does not have significant change, as shown in Figure 13.
Embodiment 9：The reactive oxygen species ROS of the high expressing cells of Epigallo-catechin gallate (EGCG) EGCG increase ER- α 36
The stomach signet ring cell cancer cell GCSR-1-6 of the high expression of ER- α 36 add respective concentration EGCG (0,6.25,12.5,
25,50 μ g/ml) after processing cell 16h, PBS is washed once.37 DEG C, 5%CO2Under the conditions of, 100nMRed
CMXRos dyeings 30min.After incubation terminates, washed once with preheating PBS, Lecia DMI4000B fluorescence microscopes are taken pictures note
Record.As a result show, cell fluorescence signal is remarkably reinforced after EGCG processing, shows ROS increases, as shown in Figure 10.
Embodiment 10：The high expressing cell apoptosis of Epigallo-catechin gallate (EGCG) EGCG induction ER- α 36
The stomach signet ring cell cancer cell GCSR-1-6 of the high expression of ER- α 36 add respective concentration EGCG (0,6.25,12.5,
25,50 μ g/ml) after processing cell 48h, washed twice with without EDTA collected by trypsinisation cells, ice PBS, 4 DEG C, 2000x g
Centrifuge 5min.Illustrate by BD PE-AnnexinV/7-AAD apoptosis detection kit, often pipe adds 100 μ l 1X Binding
Buffer is resuspended, and often pipe adds 5 μ l PE-Annexin V and 5 μ l PI, mixes.Lucifuge, it is incubated at room temperature 15 minutes.Incubation terminates
Afterwards, add 400 μ l 1X Binding Buffer to be resuspended, machine testing in streaming.As a result show, after EGCG processing, PE-
The double positive mono- positive Q4 sections cell proportion increases of Q2 and PE-AnnexinV of AnnexinV/7-AAD, show Apoptosis increase,
As shown in Figure 11, Figure 12.
Claims (3)
1. a kind of application of Epigallo-catechin gallate (EGCG) in the medicines of targeted inhibition ERs ER- α 36 are prepared,
The structural formula of the Epigallo-catechin gallate (EGCG) is：
2. application according to claim 1, it is characterised in that the Epigallo-catechin gallate (EGCG) passes through special
Property targeting combine ER- α 36, the high expression tumour cells of suppression ER- α 36.
3. application according to claim 1, it is characterised in that the Epigallo-catechin gallate (EGCG) passes through special
Property targeting combine ER- α 36, suppress other high expressing cells of ER- α 36.
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Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN108159432A (en) * | 2017-12-19 | 2018-06-15 | 华南师范大学 | A kind of targeted nano-particle for inhibiting breast cancer and its preparation and application |
| CN114948935A (en) * | 2022-03-28 | 2022-08-30 | 厦门大学 | Gallic acid derivative nano-drug, preparation method and application |
-
2017
- 2017-09-08 CN CN201710805405.6A patent/CN107496417A/en active Pending
Non-Patent Citations (1)
| Title |
|---|
| XIAOHUA PAN等: "Estrogen receptor-α36 is involved in epigallocatechin-3-gallate induced growth inhibition of ER-negative breast cancer stem/progenitor cells", 《JOURNAL OF PHARMACOLOGICAL SCIENCES》 * |
Cited By (4)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN108159432A (en) * | 2017-12-19 | 2018-06-15 | 华南师范大学 | A kind of targeted nano-particle for inhibiting breast cancer and its preparation and application |
| CN108159432B (en) * | 2017-12-19 | 2020-12-15 | 华南师范大学 | Targeted nanoparticle for inhibiting breast cancer and preparation and application thereof |
| CN114948935A (en) * | 2022-03-28 | 2022-08-30 | 厦门大学 | Gallic acid derivative nano-drug, preparation method and application |
| CN114948935B (en) * | 2022-03-28 | 2024-05-17 | 厦门大学 | Gallic acid derivative nano-drug, preparation method and application |
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