Application of miR-24-3p expression inhibitor in preparation of anti-breast cancer products
By inhibiting TMEM9 through the expression inhibitor of miR-24-3p, the problem of insufficient treatment for triple-negative breast cancer was solved, and the quality of life and survival rate were improved.
Patent Information
- Application Number
- CN202510989747.2
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2025-07-17
- Publication Date
- 2025-09-12
AI Technical Summary
Triple-negative breast cancer has a poor prognosis, traditional treatments are limited, there is a lack of effective targeted drugs, and research on miRNA regulatory mechanisms is insufficient.
By using a miR-24-3p expression inhibitor to inhibit the expression of TMEM9, the proliferation and migration ability of triple-negative breast cancer cells are reduced, and an anti-breast cancer product is prepared.
It improves the quality of life and survival rate of patients with triple-negative breast cancer, provides new treatment strategies, and reduces the proliferation and migration ability of cells.
Smart Images
Figure CN120617293A_ABST
Abstract
Description
Technical Field
[0001] The present invention belongs to the field of biomedicine technology, and particularly relates to the application of a miR-24-3p expression inhibitor in the preparation of an anti-breast cancer product. Background Art
[0002] Non-coding RNAs (NCRNAs) are a class of RNA molecules that are transcribed from DNA but do not encode proteins. They play a key role in regulating gene expression. Among them, microRNAs (miRNAs), short and highly conserved NCRNAs, have been extensively studied and confirmed to be involved in the pathogenesis of numerous major diseases, such as malignant tumors, cardiovascular diseases, and metabolic disorders. In particular, miRNAs influence tumor development and progression by regulating the expression of related genes in various cancers, demonstrating great potential as novel therapeutic targets.
[0003] Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, with a poor prognosis and a high propensity for metastasis. Due to the lack of expression of estrogen receptor (ER), progesterone receptor (PR), and HER2, traditional endocrine therapy and targeted drugs are limited in effectiveness, resulting in a relative paucity of clinical treatment options. Therefore, in-depth research on the molecular regulatory mechanisms of TNBC, particularly the identification of key regulatory miRNAs, is crucial for developing novel targeted therapy strategies and improving patient outcomes. Summary of the Invention
[0004] To address the above problems, the present invention provides a use of a miR-24-3p expression inhibitor in the preparation of an anti-breast cancer product. The present invention found that TMEM9 can promote the proliferation and migration of triple-negative breast cancer cells MDA-MB-231, and the miR-24-3p expression inhibitor miR-24-3p inhibitor can reduce the proliferation and migration ability of MDA-MB-231 cells by inhibiting the expression of TMEM9. The miR-24-3p expression inhibitor can be used to prepare an anti-breast cancer product to achieve the treatment of breast cancer and further improve the quality of life and survival rate of patients.
[0005] To achieve the above purpose, the specific technical solutions of the present invention are as follows: A first aspect of the present invention provides a use of a miR-24-3p expression inhibitor in the preparation of an anti-breast cancer product.
[0006] Furthermore, the miR-24-3p expression inhibitor is used to inhibit the proliferation of breast cancer cells.
[0007] Furthermore, the miR-24-3p expression inhibitor is used to inhibit the migration of breast cancer cells.
[0008] Furthermore, the breast cancer cells are triple-negative breast cancer cells.
[0009] Furthermore, the miR-24-3p expression inhibitor is a miR-24-3p inhibitor, and the sequence of miR-24-3p inhibitor is shown in SEQ ID NO.1.
[0010] Furthermore, the anti-breast cancer product is a small molecule drug.
[0011] Furthermore, the dosage form of the drug is an oral preparation or an injection.
[0012] The second aspect of the present invention provides an anti-breast cancer drug, which is composed of the above-mentioned miR-24-3p expression inhibitor and a solvent.
[0013] Furthermore, the miR-24-3p expression inhibitor is a miR-24-3pinhibitor with a sequence as shown in SEQ ID NO.1, the drug contains miR-24-3p inhibitor as the only effective active ingredient, and the concentration of miR-24-3pinhibitor in the drug is 37.5nM~20μM.
[0014] Furthermore, the solvent is DEPC water.
[0015] Compared with the prior art, the present invention has the following beneficial effects: The present invention provides a use of a miR-24-3p expression inhibitor in the preparation of an anti-breast cancer product. Experiments in the present invention have found that TMEM9 can promote the proliferation and migration of triple-negative breast cancer cells (MDA-MB-231). TMEM9 expression levels are high in breast cancer patients, and patients with high TMEM9 expression have a poor prognosis. However, a miR-24-3p expression inhibitor, miR-24-3 inhibitor, can further reduce the proliferation and migration ability of MDA-MB-231 cells by inhibiting TMEM9 expression. Therefore, a miR-24-3p expression inhibitor can be used to prepare an anti-breast cancer product. BRIEF DESCRIPTION OF THE DRAWINGS
[0016] In order to more clearly illustrate the embodiments of the present invention or the technical solutions in the prior art, the following briefly introduces the drawings required for use in the embodiments or the description of the prior art. Obviously, the drawings described below are only some embodiments of the present invention. For ordinary technicians in this field, other drawings can be obtained based on these drawings without paying any creative work.
[0017] Figure 1 Figure 2 shows the expression of TMEM9 in breast cancer and its relationship with overall survival (OS) and recurrence-free survival (RFS). Figure A shows the expression of TMEM9 in breast cancer and adjacent tissues using the GEPIA2 database. * indicates P <0.05; Figure B shows the relationship between TMEM9 expression and OS in GSE1456-GPL97 using the BCIP database; Figure C shows the relationship between TMEM9 expression and RFS in GSE1456-GPL97 using the BCIP database.
[0018] Figure 2 To construct the results of the assay for stably overexpressing TMEM9, Figure A shows the expression of TMEM9 in four breast cancer cell lines, MDA-MB-231, MDA-MB-453, MDA-MG-468, and HS578T, detected by immunoblotting; Figure B shows the expression of TMEM9 in four breast cancer cell lines, MDA-MB-231, MDA-MB-453, MDA-MG-468, and HS578T, detected by qPCR. TMEM9 back TMEM9 mRNA expression, *** indicates P <0.001; Figure C shows the protein level of TMEM9 after overexpression of TMEM9 detected by immunoblotting.
[0019] Figure 3 The effect of overexpression of TMEM9 on the proliferation of MDA-MB-231 cells was detected in the clone formation experiment. Figure A shows the proliferation of cells in the NC group, Figure B shows the proliferation of cells in the OE-TMEM9 group, and Figure C shows the statistical diagram of the effect of TMEM9 overexpression on cell proliferation. *** indicates P <0.001.
[0020] Figure 4 Figure 3 shows the effect of TMEM9 overexpression on apoptosis of MDA-MB-231 cells. Figure A shows the detection of cell apoptosis by flow cytometry. The upper sample of Figure A is the cell of NC group, and the lower sample of Figure A is the cell of OE-TMEM9 group. Figure B shows the effect of TMEM9 overexpression on the cell apoptosis rate. ns indicates no significant difference.
[0021] Figure 5Transwell migration assay to detect the effect of overexpression of TMEM9 on the migration ability of MDA-MB-231 cells. Figure A shows the migration of cells in the NC group, Figure B shows the migration of cells in the OE-TMEM9 group, and Figure C shows the statistical diagram of the effect of TMEM9 overexpression on cell migration ability. * indicates P <0.05, scale bar 100 μm.
[0022] Figure 6 Figure 2 Effects of transfection of miR-24-3p inhibitor on TMEM9 mRNA and protein expression in MDA-MB-231 cells. Panel A shows the expression of TMEM9 mRNA detected by qPCR; Panel B shows the expression of TMEM9 protein detected by immunoblotting. Groups: NC represents the negative control group; OE-TMEM9+Con represents the negative control group overexpressing TMEM9 and transfected with miR-24-3p inhibitor; OE-TMEM9+miR-IN represents the group overexpressing TMEM9 and transfected with miR-24-3p inhibitor. ** represents P <0.01, *** indicates P <0.001.
[0023] Figure 7 To detect the effect of transfection of miR-24-3p inhibitor on cell proliferation in MDA-MB-231 cells in a clone formation experiment, Figure A shows the cell proliferation of the NC group (negative control group), Figure B shows the cell proliferation of the OE-TMEM9+Con group (overexpression of TMEM9 and transfection of miR-24-3p inhibitor, negative control group), and Figure C shows the cell proliferation of the OE-TMEM9+miR-IN group (overexpression of TMEM9 and transfection of miR-24-3p inhibitor). Figure D is a statistical graph of cell proliferation in the NC group, OE-TMEM9+Con group, and OE-TMEM9+miR-IN group. * indicates P <0.05, ** indicates P <0.01.
[0024] Figure 8Transwell migration assay was used to detect the effect of transfection of miR-24-3p inhibitor on cell migration ability in MDA-MB-231 cells. Figure A shows the cell migration of the NC group (negative control group), Figure B shows the cell migration of the OE-TMEM9+Con group (overexpression of TMEM9 and transfection of miR-24-3p inhibitor, negative control group), and Figure C shows the cell migration of the OE-TMEM9+miR-IN group (overexpression of TMEM9 and transfection of miR-24-3p inhibitor). Figure D is a statistical graph of the cell migration ability of the NC group, OE-TMEM9+Con group, and OE-TMEM9+miR-IN group. *** indicates P <0.001, scale bar 100 μm. DETAILED DESCRIPTION
[0025] The specific embodiments of the present invention are described in detail below, but it should be understood that the scope of protection of the present invention is not limited by the specific embodiments. Based on the embodiments in the present invention, all other embodiments obtained by those of ordinary skill in the art without making creative work are within the scope of protection of the present invention. The experimental methods described in the embodiments of the present invention are conventional methods unless otherwise specified, and the materials, reagents, etc. used in the following embodiments can be obtained from commercial sources unless otherwise specified.
[0026] Triple-negative breast cancer is the most aggressive subtype of breast cancer, with a poor prognosis and a high propensity to metastasize. Traditional endocrine therapy and targeted drugs have limited efficacy, and clinical treatment options are relatively scarce. Among various cancers, miRNAs influence the occurrence and development of tumors by regulating the expression of related genes, showing great potential as new therapeutic targets. Therefore, in-depth research on the molecular regulatory mechanisms of triple-negative breast cancer and the identification of miRNAs with key regulatory roles are of great significance for developing new targeted treatment strategies and improving patient prognosis.
[0027] The present invention provides a use of a miR-24-3p expression inhibitor in the preparation of an anti-breast cancer product. Experiments in the present invention have found that TMEM9 can promote the proliferation and migration of triple-negative breast cancer cells (MDA-MB-231). TMEM9 expression levels are high in breast cancer patients, and patients with high TMEM9 expression have a poor prognosis. However, a miR-24-3p expression inhibitor, miR-24-3 inhibitor, can further reduce the proliferation and migration ability of MDA-MB-231 cells by inhibiting TMEM9 expression. Therefore, a miR-24-3p expression inhibitor can be used to prepare an anti-breast cancer product.
[0028] Example 1: Application of miR-24-3p expression inhibitor in the preparation of anti-breast cancer products 1. Materials and Methods 1.1 Materials 1.1.1 Cell line: Human breast cancer MDA-MB-231 cells were purchased from the Cell Resource Center of the Institute of Basic Medicine, Chinese Academy of Medical Sciences, Peking Union Medical College.
[0029] 1.1.2 Main Reagents RPMI 1640 medium (Hyclone, USA); fetal bovine serum (Suzhou Shuanglu Biotechnology Co., Ltd.); trypsin cell digestion buffer, BCA kit, and RIPA lysis buffer (Shanghai Biyuntian Biotechnology Co., Ltd.); protease inhibitors (Shanghai Yazyme Biopharmaceutical Technology Co., Ltd.); overexpression lentivirus (LV5-TMEM9 homo, Shanghai Jima Pharmaceutical Technology Co., Ltd.); RNAfast200 total RNA rapid extraction kit (Shanghai Feijie Biotechnology Co., Ltd.); reverse transcription kit (Suzhou Jinan Protein Technology Co., Ltd.); qPCR kit (Suzhou Jinan Protein Technology Co., Ltd.); Transwell chamber (Corning, USA); Lipofectamine™ 3000 transfection reagent (Thermo Fisher Scientific, USA); microRNA inhibitors (Shanghai Jima Pharmaceutical Technology Co., Ltd.); TMEM9 antibody (Abcam Shanghai Trading Co., Ltd.); anti-β-actin antibody (Wuhan Sanying Biotechnology Co., Ltd.); PVDF membrane (Millipore Biotechnology Co., Ltd., USA); ECL luminescent solution (Millipore Biotechnology Co., Ltd., USA); apoptosis detection kit (Shenzhen Dakoway Biotechnology Co., Ltd.).
[0030] 1.2 Experimental Methods 1.2.1 Cell Culture MDA-MB-231 cells were cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS) and 1% anti-antibody (antibody) at 37°C in a humidified atmosphere of 5% v / v CO. Cells were passaged when the cell density reached 90% for subsequent experiments.
[0031] 1.2.2 Lentiviral infection of cells TMEM9 was overexpressed in MDA-MB-231 cells using lentiviral technology. Well-growing cells were selected, digested, and resuspended in a cell suspension. The cells were seeded into 6-well plates. After 24 hours, when the cell density reached 70%–90%, TMEM9 was overexpressed using lentiviral technology. The experiment was divided into a negative control (NC) and an overexpression (OE) group. The medium was replaced 12 hours later. 48 hours after infection, when the cell density reached approximately 100%, 1µg / mL puromycin was added for selection. Selection was continued for one week, and surviving cells in the negative control and overexpression groups were passaged for future use.
[0032] 1.2.3. Transfection of cells with microRNA inhibitor Siha cells overexpressing TMEM9 were transfected with a microRNA inhibitor. 24 hours before transfection, the cells were seeded in 6-well plates so that the cell density reached 30%-50% on the next day. The sequence of miR-24-3p inhibitor is shown in SEQ ID NO.1, and the sequence of miR-24-3p inhibitor negative control is shown in SEQ ID NO.2: SEQ ID NO.1: 5'-CUGUUCCUGCUGAACUGAGCCA-3'; SEQ ID NO. 2: 5'-CAGUACUUUUGUGUAGUACAA-3'.
[0033] Dissolve the miR-24-3p inhibitor in DEPC water to a concentration of 20 μM. Dissolve the miR-24-3p inhibitor negative control in DEPC water to a concentration of 20 μM. Then, transfection with the microRNA inhibitor was performed according to the Lipofectamine™ 3000 transfection reagent instructions (75 pmoL of the microRNA inhibitor or negative control was added to a final volume of 2 mL in a 6-well plate). Experimental groups were divided into: negative control (NC), negative control group (overexpressing TMEM9 and transfected with the miR-24-3p inhibitor) (OE-TMEM9+Con), and group (overexpressing TMEM9 and transfected with the miR-24-3p inhibitor) (OE-TMEM9+miR-IN). The medium was changed 6 hours after transfection. At 48 hours, cells were harvested, and RNA and protein were extracted to assess knockdown efficiency. The transfected cells were then used for subsequent experiments.
[0034] 1.2.4 qPCR RNA was extracted according to the instructions of the RNAfast200 total RNA rapid extraction kit, and qPCR was performed according to the qPCR kit instructions. The PCR primer sequences are shown in Table 1. GAPDH was used as an internal reference gene, and the results were calculated using the 2−∆∆Ct method. Each experiment was repeated three times.
[0035] Table 1 Primer sequences 1.2.5 Immunoblotting Cells in logarithmic growth phase were harvested, washed with PBS, and resuspended in RIPA lysis buffer mixed with protease inhibitors at a 100:1 volume ratio. After incubation on ice for 30 minutes, the cells were transferred to an EP tube and centrifuged at 12,000 g for 10 minutes at 4°C. The cell supernatant was collected, and protein was quantified using a BCA protein assay kit. SDS-PAGE electrophoresis was performed, and proteins were transferred to a PVDF membrane. The membrane was blocked with 5% w / v skim milk for 1 hour at room temperature and incubated with primary antibodies (TMEM9 and β-actin) overnight at 4°C. Subsequently, the membrane was incubated with a secondary antibody (HRP-conjugated Goat Anti-Rabbit IgG) for 1 hour at room temperature in a shaking incubator. Detection was performed using ECL chemiluminescence.
[0036] 1.2.6. Clone formation assay The cells in the logarithmic growth phase were digested, centrifuged, and resuspended to form a cell suspension. 500 cells were inoculated into each well of a 96-well plate and cultured in a cell culture incubator under 5 v / v% CO2 and saturated humidity at 37°C for 14 days. The culture medium was replaced every 3 days during this period. After the culture time, the cells were fixed with 4 v / v% paraformaldehyde for 20 minutes and stained with 0.1 v / v% crystal violet for 30 minutes. The cells were photographed and counted under a microscope. Each experiment was repeated 3 times.
[0037] 1.2.7 Cell apoptosis assay The cells were digested with EDTA-free trypsin and collected by centrifugation. The cells were then operated according to the instructions of the cell apoptosis kit and cell apoptosis was detected by flow cytometry. Each experiment was repeated three times.
[0038] 1.2.8 Transwell cell migration assay Select cells in good growth state, digest and centrifuge them, resuspend them in serum-free medium, count the cells, and inoculate 200 μL of 2×10 4For each cell, add 600 μL of complete culture medium (containing 10% v / v FBS) to the lower chamber and place the Transwell chamber in a constant temperature incubator for continued culture. After 48 hours, remove the plate and fix with 4% v / v paraformaldehyde for 20 minutes. Stain with 0.1% v / v crystal violet for 30 minutes, photograph, and count under a microscope. Repeat three times for each experiment.
[0039] 1.2.9 Bioinformatics Analysis This study used the GEPIA2 database to analyze the expression of TMEM9 in breast cancer and adjacent tissues. The BCIP database was used to analyze the relationship between TMEM9 expression and overall survival (OS) and recurrence-free survival (RFS) of breast cancer. TargetScanHuman 8.0 software was used to predict microRNAs that interact with TMEM9.
[0040] 1.2.10 Statistical Analysis The results were expressed as mean ± standard deviation. Two-sample test was performed by t test, multiple samples were tested by analysis of variance, and two-sided test was performed by P A difference of <0.05 was defined as statistically significant, and SPSS 21.0 software was used for statistical analysis.
[0041] 2 Results 2.1. TMEM9 expression in breast cancer and its relationship with OS and RFS like Figure 1 As shown in the results, GEPIA2 database analysis revealed that the expression level of TMEM9 in breast cancer (1085 cases) was higher than that in adjacent tissues (291 cases); and patients with high TMEM9 expression had shorter OS and RFS, which suggested that TMEM9 may be involved in the occurrence of breast cancer and may be a marker for poor prognosis in breast cancer patients.
[0042] 2.2. Construction of cell lines stably overexpressing TMEM9 The present invention firstly uses immunoblotting technology to detect the expression of TMEM9 in four breast cancer cells, namely MDA-MB-231, MDA-MB-453, MDA-MG-468 and HS578T. The results show that the expression level of TMEM9 in MDA-MB-231 and HS578T cells is relatively low ( Figure 2 A), the present invention subsequently conducted subsequent research using MDA-MB-231 cells as the research object.
[0043] By using lentiviral technology to overexpress TMEM9 in MDA-MB-231 cells, the results showed that compared with the negative control group, the overexpression group TMEM9 The mRNA expression level ( Figure 2 B) and TMEM9 protein ( Figure 2 C) The expression level was significantly increased, indicating that a cell line stably overexpressing TMEM9 was successfully constructed.
[0044] 2.3 Overexpression of TMEM9 promotes proliferation of MDA-MB-231 cells The effect of overexpression of TMEM9 on the proliferation of MDA-MB-231 cells was detected by clone formation assay. The results showed that overexpression of TMEM9 increased the number of MDA-MB-231 cell clones, suggesting that overexpression of TMEM9 promoted the proliferation of MDA-MB-231 cells. Figure 3 ); Furthermore, apoptosis assay was used to detect the effect of overexpression of TMEM9 on the proliferation and apoptosis of MDA-MB-231 cells. The results showed that there was no statistically significant difference in the apoptosis rate after overexpression of TMEM9 ( Figure 4 ).
[0045] 2.4 Overexpression of TMEM9 promotes the migration of MDA-MB-231 cells Transwell migration assay was used to detect the changes in the migration ability of MDA-MB-231 cells after overexpression of TMEM9. The results showed that the number of MDA-MB-231 cells that passed through the membrane increased after overexpression of TMEM9, suggesting that overexpression of TMEM9 promotes the migration of MDA-MB-231 cells. Figure 5 ).
[0046] 2.5 Prediction of microRNAs interacting with TMEM9 To further explore the reasons for the high expression of TMEM9 in breast cancer, TargetScanHuman 8.0 software was used to predict microRNAs that interact with TMEM9. The results showed that miR-24-3p may be the microRNA that interacts with TMEM9.
[0047] 2.6 Effects of miR-24-3p inhibitor on TMEM9 mRNA and protein expression To further verify the interaction between miR-24-3p and TMEM9, the present invention detected the mRNA and protein expressions of TMEM9 after transfecting miR-24-3p inhibitor into TMEM9-overexpressing cells.
[0048] The results showed that after overexpression of TMEM9 and simultaneous transfection of miR-24-3p inhibitor (OE-TMEM9+miR-IN) in MDA-MB-231 cells, the mRNA expression of TMEM9 was significantly decreased (P<0.05). Figure 6 A) and protein ( Figure 6 B) The expression level of miR-24-3p was lower than that of the TMEM9 overexpression group, suggesting that miR-24-3p may be involved in regulating the expression of TMEM9.
[0049] 2.7 Effect of transfection of miR-24-3p inhibitor on cell proliferation in MDA-MB-231 cells To further verify the effect of miR-24-3p on TMEM9 function, the present invention detected changes in cell proliferation ability after transfecting miR-24-3p inhibitor into TMEM9-overexpressing MDA-MB-231 cells.
[0050] like Figure 7 As shown, the clone formation results showed that the number of clones formed increased after overexpression of TMEM9 (OE-TMEM9+Con) in MDA-MB-231 cells; the number of clones formed decreased after overexpression of TMEM9 and simultaneous transfection of miR-24-3p inhibitor (OE-TMEM9+miR-IN), suggesting that TMEM9 promotes cell proliferation and miR-24-3p is involved in regulating the pro-proliferation effect of TMEM9.
[0051] 2.8 Effect of transfection of miR-24-3p inhibitor on cell migration ability in MDA-MB-231 cells To further verify the effect of miR-24-3p on TMEM9 function, the present invention detected changes in cell migration ability after transfecting miR-24-3p inhibitor into TMEM9-overexpressing MDA-MB-231 cells.
[0052] like Figure 8 As shown, the Transwell results showed that the number of transmembrane cells increased after overexpression of TMEM9 (OE-TMEM9+Con) in MDA-MB-231 cells, reflecting the enhanced cell migration ability; the number of transmembrane cells decreased after overexpression of TMEM9 and simultaneous transfection of miR-24-3p inhibitor (OE-TMEM9+miR-IN), suggesting that TMEM9 promotes cell migration and miR-24-3p is involved in regulating the pro-migratory effect of TMEM9.
[0053] It should be noted that when numerical ranges are mentioned in the present invention, it should be understood that both endpoints of each numerical range and any value between the two endpoints may be selected. Since the steps and methods used are the same as those in the embodiments, in order to avoid redundancy, the present invention describes preferred embodiments. Although preferred embodiments of the present invention have been described, those skilled in the art may make additional changes and modifications to these embodiments once they understand the basic inventive concepts. Therefore, the appended claims are intended to be interpreted as including the preferred embodiments and all changes and modifications that fall within the scope of the present invention.
[0054] Obviously, those skilled in the art may make various changes and modifications to the present invention without departing from the spirit and scope of the present invention. Thus, if such changes and modifications fall within the scope of the claims and their equivalents, the present invention is intended to include such changes and modifications.
Claims
1. Application of miR-24-3p expression inhibitors in the preparation of anti-breast cancer products.
2. The use according to claim 1, characterized in that The miR-24-3p expression inhibitor is used to inhibit the proliferation of breast cancer cells.
3. The use according to claim 1, characterized in that The miR-24-3p expression inhibitor is used to inhibit the migration of breast cancer cells.
4. The use according to claim 2 or claim 3, characterized in that The breast cancer cells are triple-negative breast cancer cells.
5. The use according to claim 1, characterized in that The miR-24-3p expression inhibitor is a miR-24-3p inhibitor, and the sequence of the miR-24-3p inhibitor is shown in SEQ ID NO.
1.
6. The use according to claim 1, characterized in that The anti-breast cancer product is a small molecule drug.
7. The use according to claim 1, characterized in that The dosage form of the medicine is oral preparation or injection.
8. An anti-breast cancer drug, characterized in that: The drug consists of the miR-24-3p expression inhibitor according to claim 1 and a solvent.
9. The drug according to claim 8, characterized in that The miR-24-3p expression inhibitor is a miR-24-3p inhibitor having a sequence as shown in SEQ ID NO.1, and the concentration of the miR-24-3p inhibitor in the drug is 37.5 nM to 20 μM.
10. The drug according to claim 8, characterized in that The solvent is DEPC water.