Application of Indanone Sesquiterpenoids in the Preparation of Antitumor Drugs

Abstract

The present invention belongs to the technical field of anti-tumor drug research, and particularly relates to the application of an indanone sesquiterpene compound or an extract containing the same in the preparation of anti-tumor drugs. The structure of the indanone sesquiterpene compound is shown in Formula I. Through experimental verification, the indanone sesquiterpene compound can inhibit the proliferation of breast cancer cells, human renal clear cell adenocarcinoma cells, esophageal cancer cells and glioma tumor cells, indicating that the indanone sesquiterpene compound provided by the present invention has the potential to be prepared into anti-tumor drugs; R1 is selected from a hydrogen atom or a methyl group, R2 is selected from a hydrogen atom or a hydroxyl group, R3 is selected from any one of hydrogen, hydroxyl or glycoside, R4 is selected from hydrogen or acetyl, and R5 is selected from any one of hydrogen, methyl, hydroxyl or glycoside.

Description

Technical Field

[0001] The present invention belongs to the technical field of anti-tumor drug research, and particularly relates to the application of an indanone sesquiterpene compound or an extract containing the same in the preparation of an anti-tumor drug. Background Art

[0002] Triple-negative breast cancer (TNBC) patients are negative for estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2. It is a subtype of breast cancer, accounting for 15% - 20% of primary breast cancer. TNBC is characterized by high invasiveness, high metastasis rate, high risk of recurrence and metastasis, etc., with a relatively high mortality rate, and is prone to occur in young women. Due to the lack of effective action targets, TNBC has unsatisfactory effects on endocrine therapy and molecular targeted therapy currently used in clinical practice and will develop serious drug resistance. Therefore, discovering new anti-TNBC small molecule drugs or lead compounds has very important clinical significance and value.

[0003] Pteris wallichiana is a large terrestrial plant. It is a medium to large fern in the genus Pteris, section Reticulatae, series Tripartitae. The whole herb is used as medicine, slightly bitter, astringent, and cool. It has the effects of clearing heat and stopping bleeding. It is used for dysentery, infantile convulsion, and traumatic bleeding. Pteris wallichiana contains various anti-inflammatory, antibacterial, antiviral, anti-diabetic and other components, but there has been no report on whether it contains anti-tumor components. Summary of the Invention

[0004] In view of the above problems, the present invention provides the application of an indanone sesquiterpene compound or an extract containing the same in the preparation of an anti-tumor drug. Through experimental verification, the indanone sesquiterpene compound can inhibit the proliferation of breast cancer cells, human renal clear cell adenocarcinoma cells, and glioma tumor cells, indicating that the indanone sesquiterpene compound provided by the present invention has the potential to be prepared into an anti-tumor drug.

[0005] The specific technical solution provided by the present invention is as follows:

[0006] In the first aspect of the present invention, there is provided the application of an indanone sesquiterpene compound or an extract containing the same in the preparation of an anti-tumor drug, and the structure of the indanone sesquiterpene compound is shown as formula I:

[0007]

[0008] Wherein, R1 is selected from a hydrogen atom or a methyl group, R2 is selected from a hydrogen atom or a hydroxyl group, R3 is selected from any one of hydrogen, a hydroxyl group, or a glycoside, R4 is selected from hydrogen or an acetyl group, and R5 is selected from any one of hydrogen, a methyl group, a hydroxyl group, or a glycoside.

[0009] As a preferred embodiment of the present invention, the structure of the indanone sesquiterpene compound is shown as any one of formulas II - IV:

[0010]

[0011] As a preferred embodiment of the present invention, the indanone sesquiterpenoid compound or an extract containing the same is used for preparing a drug for treating breast cancer, kidney cancer, esophageal cancer or glioblastoma multiforme.

[0012] As a preferred embodiment of the present invention, the indanone sesquiterpenoid compound or an extract containing the same is used for preparing a drug for inhibiting the proliferation of tumor cells.

[0013] As a preferred embodiment of the present invention, the tumor cells are breast cancer cells EMT-6 and 4T1, human renal clear cell adenocarcinoma cells 786O, esophageal cancer cells TE10 or glioma cells U87.

[0014] As a preferred embodiment of the present invention, the concentrations of the indanone sesquiterpenoid compound shown in Formula II for inhibiting the proliferation of breast cancer cells EMT-6 and 4T1 are both 5 μg / ml to 10 μg / ml, the concentrations for inhibiting human renal clear cell adenocarcinoma cells 786O and glioma cells U87 are 12 μg / ml to 24 μg / ml, and the concentration for inhibiting esophageal cancer cells TE10 is 20 μg / ml to 30 μg / ml;

[0015] The concentrations of the indanone sesquiterpenoid compound shown in Formula III for inhibiting the proliferation of breast cancer cells EMT-6 and 4T1 are both 5 μg / ml to 10 μg / ml, the concentrations for inhibiting human renal clear cell adenocarcinoma cells 786O and glioma cells U87 are 12 μg / ml to 20 μg / ml, and the concentration for inhibiting esophageal cancer cells TE10 is 20 μg / ml to 30 μg / ml;

[0016] The concentrations of the indanone sesquiterpenoid compound shown in Formula IV for inhibiting esophageal cancer cells TE10 and glioma cells U87 are both 20 μg / ml to 30 μg / ml, and the concentration for inhibiting human renal clear cell adenocarcinoma cells 786O is 30 μg / ml to 40 μg / ml.

[0017] As a preferred embodiment of the present invention, the extract containing the indanone sesquiterpenoid compound is prepared according to the following steps:

[0018] Using methanol as an extraction solvent, extracting Pteris wallichiana, and obtaining an extraction paste after recovering the solvent from the extract;

[0019] Successively extracting the extraction paste with petroleum ether, dichloromethane and ethyl acetate, collecting the dichloromethane extraction part and the ethyl acetate extraction part, and the extract containing the indanone sesquiterpenoid compound is the dichloromethane extraction part or the ethyl acetate extraction part or any proportion mixture of the two.

[0020] In a second aspect of the present invention, there is provided an anti-tumor drug, which comprises the indanone sesquiterpenoid compound or an extract containing the same, and a pharmaceutically acceptable excipient or carrier.

[0021] As a preferred embodiment of the present invention, the drug is prepared into an oral preparation or an injection preparation.

[0022] As a preferred embodiment of the present invention, the oral preparation is a capsule, a tablet, a granule or a liquid preparation.

[0023] As a preferred embodiment of the present invention, the injection preparation is an injection solution or an injection powder.

[0024] Compared with the prior art, the beneficial effects of the present invention are as follows:

[0025] The present invention provides the use of an indanone sesquiterpenoid compound or an extract containing the same in the preparation of an anti-tumor drug. Through experimental verification, the indanone sesquiterpenoid compound provided by the present invention can inhibit the proliferation of breast cancer cells EMT-6 and 4T1, human renal clear cell adenocarcinoma cells 786O, esophageal cancer TE10 or glioma cells U87. BRIEF DESCRIPTION OF THE DRAWINGS

[0026] Figure 1 is the flow chart of the isolation and purification of Pteris wallichiana;

[0027] Figures 2 - 3 shows the effects of the petroleum ether extraction fraction, dichloromethane extraction fraction, ethyl acetate extraction fraction and methanol extraction fraction on the proliferation of EMT-6 and 4T1 cells; **** P < 0.0001;

[0028] Figure 4 shows that Fr.EA-2 and Fr.EA-3 significantly inhibit the proliferation of EMT-6 and 4T1 cells; **** P < 0.0001;

[0029] Figure 5 shows that Fr.DCM-1 and Fr.DCM-8 significantly inhibit the proliferation of EMT-6 and 4T1 cells; **** P < 0.0001;

[0030] Figure 6 shows the 24h IC 50 value of Fr.EA-2 on EMT-6 cells;

[0031] Figure 7 shows the 24h IC 50 value of Fr.DCM-8 on EMT-6 cells;

[0032] Figure 8 is the IC value of Fr.EA-2-4 against EMT-6 and 4T1 50 value;

[0033] Figure 9 is the IC value of Fr.DCM-8-3 against EMT-6 and 4T1 50 value;

[0034] Figure 10 is the IC value of pterosin B inhibiting the proliferation of EMT-6 and 4T1 cells 50 value;

[0035] Figure 11 is the IC value of pterosin B inhibiting the proliferation of renal cancer cell line 786O, esophageal cancer cell line TE10 and glioma cell line U87 50 value; **** P < 0.0001;

[0036] Figure 12 is the IC value of pterosin A inhibiting the proliferation of EMT-6 and 4T1 cells 50 value;

[0037] Figure 13 is the IC value of pterosin A inhibiting the proliferation of renal cancer cell line 786O, esophageal cancer cell line TE10 and glioma cell line U87 50 value; **** P < 0.0001;

[0038] Figure 14 is the IC value of 14-acetyl-pterosin C 3-O-β-D-glucosidede inhibiting the proliferation of renal cancer cell line 786O, esophageal cancer cell line TE10 and glioma cell line U87 50 value; **** P < 0.0001;

[0039] Figure 15 is to detect the effect of pterosin B on tumor cell proliferation by scratch assay;

[0040] Figure 16 is to detect the effect of pterosin A on tumor cell proliferation by scratch assay;

[0041] Figure 17 is to observe the radiosensitivity of pterosin B to EMT-6 and 4T1 cells by increasing radiation;

[0042] Figure 18 is to observe the radiosensitivity of pterosin A to EMT-6 and 4T1 cells by increasing radiation;

[0043] Figure 19 is the effect of pterosin B on the proliferation of paclitaxel-resistant cell lines EMT-6-R and 4T1-R;

[0044] Figure 20 Effect of pterosin A on the proliferation of paclitaxel-resistant cell lines EMT-6-R and 4T1-R;

[0045] Figure 21 Detection of intracellular reactive oxygen species level under the intervention of pterosin B by DCFH-DA probe method;

[0046] Figure 22 Detection of intracellular reactive oxygen species level under the intervention of pterosin A by DCFH-DA probe method;

[0047] Figure 23 Pterosin B significantly inhibits tumor growth in tumor-bearing mice; each row has 6 parallels;

[0048] Figure 24 Change of tumor volume in tumor-bearing mice under the intervention of pterosin B;

[0049] Figure 25 Pterosin A significantly inhibits tumor growth in tumor-bearing mice; each row has 6 parallels;

[0050] Figure 26 Change of tumor volume in tumor-bearing mice under the intervention of pterosin A. Detailed implementation mode

[0051] The present invention will be further described below in conjunction with specific embodiments.

[0052] The present invention provides an application of an indanone sesquiterpene compound or an extract containing the same in the preparation of an anti-tumor drug. The structure of the indanone sesquiterpene compound is shown in Formula I:

[0053]

[0054] Among them, R1 is selected from a hydrogen atom or a methyl group, R2 is selected from a hydrogen atom or a hydroxyl group, R3 is selected from any one of hydrogen, hydroxyl group or glycoside, R4 is selected from hydrogen or acetyl group, and R5 is selected from any one of hydrogen, methyl group, hydroxyl group or glycoside.

[0055] Through experimental verification, the indanone sesquiterpene compound provided by the present invention has an anti-tumor effect, especially has a better improvement effect on breast cancer, kidney cancer, esophageal cancer and glioma. The indanone sesquiterpene compound can inhibit the proliferation of breast cancer cells EMT-6 and 4T1, human renal clear cell adenocarcinoma cells 786O, esophageal cancer TE10 or glioma cells U87.

[0056] The above extract containing the indanone sesquiterpene compound can be extracted from Pteris wallichiana. The operation process is as follows:

[0057] Using methanol as the extraction solvent, extract Pteris wallichiana, and obtain an extraction paste after recovering the solvent from the extract;

[0058] The extraction extract was successively extracted with petroleum ether, dichloromethane and ethyl acetate, and the dichloromethane extraction part and the ethyl acetate extraction part were collected. The extract containing indanone sesquiterpenoids was the dichloromethane extraction part or the ethyl acetate extraction part or any proportion mixture of the two.

[0059] Example 1

[0060] Extraction and Separation of Indanone Sesquiterpenoids from Pteris wallichiana

[0061] 1. Crude extraction of indanone sesquiterpenoids

[0062] Take 30 kg of dry roots of Pteris wallichiana, extract with methanol by heating under reflux for 3 times, combine the filtrates after recovering the solvent to obtain 9 kg of methanol extraction extract, and disperse the extract with pure water.

[0063] Extract successively with petroleum ether, dichloromethane and ethyl acetate to obtain 340 g of petroleum ether extraction part, 890 g of dichloromethane extraction part, and 2 kg of ethyl acetate extraction part.

[0064] 2. Screening of active parts

[0065] Count the tumor cells EMT-6, 4T1 cells, glioma cells U87 and renal cancer cells 786O in the logarithmic growth phase respectively, and prepare a cell suspension with a concentration of 6×10 4 cells / mL. Pipette 100 μL and add it to a 96-well plate, and culture overnight in a cell incubator at 37 °C and 5% CO2. After the cells adhered, add the above petroleum ether extraction part, dichloromethane extraction part and ethyl acetate extraction part, and the concentration gradients were: 1000 μg / ml, 750 μg / ml, 500 μg / ml, 250 μg / ml. Set 3 replicates for each group, and the drug solvent was used as the control group. After culturing for 48 h, add 10 μL of CCK-8 working solution, continue to incubate in the cell incubator for 3 h, and detect and calculate the OD value at 450 nm.

[0066] The results are as Figures 2 - 3 shown. It can be obtained from Figures 2 - 3 that both the dichloromethane (DCM) and ethyl acetate (EA) extraction parts significantly inhibited the proliferation of EMT-6 and 4T1 cells. In addition, when the concentration of the DCM and EA extraction parts was 250 μg / ml, they also had a certain inhibitory effect on the proliferation of glioma cells U87 and renal cancer cells 786O.

[0067] 3. Isolation and purification

[0068] The dichloromethane and ethyl acetate extraction parts were dissolved in methanol respectively, and 100-200 mesh silica gel was added in a weight ratio of 1:1.5 to mix the sample, and the sample was subjected to normal phase silica gel column chromatography, with the eluent being dichloromethane:methanol=100-0:0-100. The same components were combined by thin layer plate detection to obtain 8 components Fr.DCM-1, Fr.DCM-2, Fr.DCM-3, Fr.DCM-4, Fr.DCM-5, Fr.DCM-6, Fr.DCM-7, Fr.DCM-8 under the dichloromethane extraction part, and 4 components Fr.EA-1, Fr.EA-2, Fr.EA-3, Fr.EA-4 under the ethyl acetate extraction part. Specific separation and purification process detection Figure 1 .

[0069] The 12 components were tested by CCK8 cell proliferation assay. The concentrations of Fr.DCM-1, Fr.DCM-2, Fr.DCM-3, Fr.DCM-4, Fr.DCM-5, Fr.DCM-6, Fr.DCM-7, and Fr.DCM-8 were all 250 μg / ml, and the concentrations of Fr.EA-1, Fr.EA-2, Fr.EA-3, and Fr.EA-4 were all 100 μg / ml. The results are shown in Figures 4 - 5 shown.

[0070] The results showed that Fr.EA-2, Fr.EA-3, Fr.DCM-1 and Fr.DCM-8 significantly inhibited the proliferation of EMT-6 and 4T1 cells.

[0071] Continue to dilute Fr.EA-2, Fr.EA-3, Fr.DCM-1 and Fr.DCM-8 in a gradient concentration to obtain 200μg / ml, 160μg / ml, 80μg / ml, 40μg / ml, 20μg / ml, 10μg / ml, and 5μg / ml, and act on EMT-6 and 4T1 cells for 24h. CCK8 was used to detect cell proliferation activity, and the IC value of Fr.EA-2 on EMT-6 cells for 24h was obtained. 50 The IC values ​​of Fr.DCM-8 for EMT-6 cells at 24 h were 12.58 μg / ml and 9.26 μg / ml, respectively. 50 14.75 and 16.31 μg / ml respectively, see Figures 6 - 7 .

[0072] Fr.EA-2 was subjected to silica gel column chromatography, 200-300 mesh silica gel was mixed with the sample, and the eluent was dichloromethane:ethyl acetate = 30:1-5:1, and five components, Fr.EA-2-1, Fr.EA-2-2, Fr.EA-2-3, Fr.EA-2-4, and Fr.EA-2-5, were obtained. Among them, Fr.EA-2-4 had an IC of 0.0447 for EMT-6 and 4T1. 50The values are 9.46 μg / ml and 9.87 μg / ml respectively, see Figure 8 .

[0073] Perform silica gel column chromatography on Fr.DCM-8, mix the sample with silica gel of 200-300 mesh, and the eluent is dichloromethane:ethyl acetate = 15-1:1, obtaining six components: Fr.DCM-8-1, Fr.DCM-8-2, Fr.DCM-8-3, Fr.DCM-8-4, Fr.DCM-8-5 and Fr.DCM-8-6. Among them, the IC 50 values of Fr.DCM-8-3 for EMT-6 and 4T1 are 8.18 and 8.64 μg / ml respectively, see Figure 9 .

[0074] Separate and purify Fr.EA-2-4 by semi-preparative liquid phase. The chromatographic column is YMC liquid chromatographic column ODS, 5 μm, detect at 200 mm, and the eluent is isocratic elution of methanol and water according to the volume ratio of 94:100. The main chemical component pterosin B in Fr.EA-2-4 is obtained, and its structural formula is as follows:

[0075]

[0076] Separate and purify Fr.DCM-8-3 by semi-preparative liquid phase. The chromatographic column is YMC liquid chromatographic column ODS, 5 μm, detect at 200 mm, and the eluent is isocratic elution of methanol and water according to the volume ratio of 90:100. The main chemical component pterosin A in Fr.DCM-8-3 is obtained, and its structural formula is as follows:

[0077]

[0078] Separate and purify Fr.DCM-8-3 by semi-preparative liquid phase. The chromatographic column is YMC liquid chromatographic column ODS, 5 μm, detect at 200 mm, and the eluent is isocratic elution of methanol and water according to the volume ratio of 85:100. The new chemical component 14-acetyl-pterosin C 3-O-β-D-glucosidede in Fr.DCM-8-3 is obtained, and its structural formula is as follows:

[0079]

[0080] Example 2

[0081] Detect the effects of pterosin B, pterosin A and the new chemical component 14-acetyl-pterosin C3-O-β-D-glucosidede on the proliferation of tumor cells by CCK8 method

[0082] Detect the proliferation of tumor cells according to the method in Example 1. The results are asFigures 10 - 14 as shown

[0083] The results showed that the IC 50 values of pterosin B against EMT-6 and 4T1 were 7.274 μg / ml and 6.175 μg / ml respectively; the IC 50 values against the proliferation of renal cancer cells 786O and glioma cells U87 were approximately 19 μg / ml. The IC 50 values of pterosin A against EMT-6 and 4T1 were 5.24 and 7.87 μg / ml respectively; the IC 50 values against the proliferation of renal cancer cells 786O and glioma cells U87 were approximately 17 μg / ml; the IC 50 value against the proliferation of esophageal cancer cells TE10 was approximately 21 μg / ml. The IC 50 value of the new chemical component 14-acetyl-pterosin C 3-O-β-D-glucosidede against the proliferation of breast cancer cells EMT-6 and 4T1 was approximately 8.45 μg / ml, and the IC 50 values against esophageal cancer cells TE10 and glioma cells U87 were both 22.3 μg / ml, and the IC 50 value against inhibiting human renal clear cell adenocarcinoma cells 786O was 33.6 μg / ml.

[0084] Example 3

[0085] Scratch assay to detect the effect of pterosin B and pterosin A on tumor cell proliferation

[0086] 1. Method

[0087] Cells in the logarithmic growth phase were seeded into a 12-well plate and cultured until the cell growth density reached 100%. The serum was discarded, a 10 μL pipette tip was used to draw a straight line on the cells, the detached cells were washed away with PBS, and then the medium was replaced with serum-free drug-containing medium supplemented with double antibiotics. The concentration of pterosin B or pterosin A in the drug-containing medium was 5 μg / ml, and observations and photographs were taken under a microscope. After 24 h, the medium was discarded and the cells were washed with PBS, and observations and photographs were taken under a microscope. The results were as Figures 15 - 16 shown.

[0088] The results showed that pterosin B and pterosin A could significantly inhibit the migration ability of EMT-6 and 4T1 cells.

[0089] Example 4

[0090] Effect of pterosin B and pterosin A on the sensitivity of tumor cells

[0091] 1. Increase the sensitivity of EMT-6 and 4T1 cells to radiation

[0092] The sensitivity of paclitaxel-resistant cell lines EMT-6-R and 4T1-R to radiation was observed by colony formation assay. The cells were irradiated with 4 Gy, and simultaneously treated with 8 μg / ml of pterosin B and pterosin A respectively, to observe whether pterosin B and pterosin A could increase the sensitivity of EMT-6 and 4T1 cell lines to radiation. The results are as Figures 17 - 18 shown.

[0093] The results showed that pterosin B and pterosin A could significantly increase the sensitivity of paclitaxel-resistant cell lines EMT-6-R and 4T1-R to radiation.

[0094] 2. Increase the sensitivity of EMT-6 and 4T1 drug-resistant cells to paclitaxel

[0095] Paclitaxel-resistant cell lines EMT-6-R and 4T1-R in the logarithmic growth phase were counted and prepared into cell suspensions with a concentration of 2 - 6×10 4 cells / mL. 100 μL was aspirated and added to a 96-well plate, and cultured overnight in a 37 °C, 5% CO2 cell incubator. After the cells adhered, 8 μg / ml of pterosin B and pterosin A were added respectively. Each group was set with 3 replicates, and the drug solvent DMSO was used as the control group, labeled as Vehicle. After culturing for 48 h, 10 μL of CCK-8 working solution was added, and the cells were incubated for another 3 h in the cell incubator. The OD value was measured at 450 nm and the cell survival rate was calculated. The results are as Figures 19 - 20 shown.

[0096] The results showed that pterosin B and pterosin A significantly increased the sensitivity of drug-resistant cell lines EMT-6-R and 4T1-R to paclitaxel.

[0097] Example 5

[0098] Detection of intracellular reactive oxygen species level by DCFH-DA probe method

[0099] EMT-6 and 4T1 cells in the logarithmic growth phase were cultured in 6-well plates. After they grew to 80% and adhered, pterosin B and pterosin A with a concentration of 8 μg / ml were used to intervene the cells for 12 h respectively. The DCFH-DA probe was diluted with serum-free medium at a ratio of 1:1000. Except for the negative control group, not less than 1 mL of DCFH-DA working solution was added to each well, and incubated at 37 °C in the dark for 20 min. Then the cells were washed 3 times with serum-free medium, and the fluorescence intensity of each group was observed under a fluorescence inverted microscope at an excitation wavelength of 488 nm, and photographed and recorded. The results are as Figures 21 - 22 shown.

[0100] The results showed that pterosin B and pterosin A could significantly induce the accumulation of reactive oxygen species in EMT-6 and 4T1 cells, and then induce apoptosis.

[0101] Example 6

[0102] Pterosin B and pterosin A significantly inhibit tumor growth in tumor-bearing mice

[0103] Take 1×10 6 ~5×10 6 logarithmic growth phase EMT-6 and 4T1 cells and subcutaneously inject them into the right axilla of BALB / c nude mice. Detect the tumor mass size every 2 days. When the tumor mass volume reaches 100 mm 3 , intraperitoneally inject the drug for treatment, once every 2 days, 10 mg / mg, 100 μL. Divide the mice into a control group, a pterosin B group, and a pterosin A group. End the treatment after 2 weeks. During this period, detect the tumor mass volume once every 2 days, and collect the tumor tissues of each group of mice for statistical analysis. The results are as Figures 23 - 26 shown.

[0104] The results show that pterosin B and pterosin A can significantly inhibit tumor growth.

[0105] The above description and display have shown the basic principles and main features of the present invention. Professionals in the field should understand that the present invention is not limited by the above embodiments. The above embodiments and descriptions only illustrate the basic principles of the present invention. Without departing from the spirit and scope of the present invention, the present invention will have various changes and improvements, and these changes and improvements all fall within the scope of the present invention claimed. The scope of the present invention claimed is defined by the appended claims and their equivalents.

Claims

1. Use of indanone sesquiterpenoid compounds in the preparation of anti-tumor drugs, characterized in that: The structure of the indanone sesquiterpenoid compound is shown in any one of the following: ； ； The indanone sesquiterpenoid compound is used for preparing medicine for treating breast cancer, kidney cancer, esophageal cancer or brain glioma.

2. The use according to claim 1, characterized in that: The indanone sesquiterpenoid compound is used for preparing a drug for inhibiting the proliferation of tumor cells.

3. The use according to claim 2, characterized in that: The tumor cells are breast cancer cells EMT-6 and 4T1, human renal clear cell adenocarcinoma cells 786O, esophageal cancer cells TE10 or glioma cells U87.

4. The use according to claim 3, characterized in that: The concentration of the indanone sesquiterpenoid compound shown in Formula III that inhibits the proliferation of breast cancer cells EMT-6 and 4T1 is 5 µg / ml~10 µg / ml, the concentration that inhibits the proliferation of human renal clear cell adenocarcinoma cells 786O and glioma cells U87 is 12 µg / ml~20 µg / ml, and the concentration that inhibits the proliferation of esophageal cancer cells TE10 is 20 µg / ml~30 µg / ml; The concentration of the indanone sesquiterpenoid compound shown in formula IV that inhibits esophageal cancer cell TE10 and glioma cell U87 is 20 µg / ml to 30 µg / ml, and the concentration that inhibits human renal clear cell adenocarcinoma cell 786O is 30 µg / ml to 40 µg / ml.

5. An anti-tumor drug, characterized in that: The drug comprises the indanone sesquiterpenoid compound according to claim 1, and a pharmaceutically acceptable adjuvant or carrier. The drug is used for preventing breast cancer, kidney cancer, esophageal cancer or brain glioma.

6. The drug according to claim 5, characterized in that The drug is prepared as an oral preparation or an injection preparation.

7. The drug according to claim 6, characterized in that The oral preparation is a capsule, tablet, granule or liquid preparation.

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