Application of CRY1 gene as target

Abstract

The invention discloses application of a CRY1 gene as a target spot. The application of the CRY1 gene as the target spot comprises the application in preparation of an animal model for tumor cell magnetic field regulation and control research or the application in preparation of a product in which the magnetic field affects the tumor cells. The animal model is constructed by knocking out the CRY1 gene or overexpressing the CRY1 gene, and the body reaction of the animal model in the magnetic field environment and the expression of the tumor cells in the magnetic field environment are studied. The application proves that the low-intensity magnetic field can regulate and control the CRY1 gene and protein in the tumor cells, and the tumor cells can sense the change of the magnetic field through the CRY1; the expression of the tumor cells CRY1 in a weak magnetic field environment is reduced, and after the CRY1 is prevented from degrading / over-expressing the CRY1, the proliferation of the tumor cells inhibited by the magnetic field and the cycle arrest of the G0 / G1 cells can be recovered.

Description

Technical Field

[0001] This application relates to the field of biomedical technology, specifically to the application of the CRY1 gene as a target. Background Technology

[0002] Cancer has become the leading cause of death worldwide. In recent years, increasing research has found that steady-state magnetic fields can inhibit tumor cell proliferation and prolong survival. Magnetic field therapy, as a non-invasive method for inhibiting tumors, has become a new concept in cancer treatment due to its advantages such as few side effects, high efficiency, and wide applicability. Therefore, in-depth analysis of the specific mechanisms of action of magnetic fields on tumor cells has significant clinical importance and application value.

[0003] Most existing magnetic field research refers to steady-state strong magnetic fields, that is, those greater than 50 μT of the Earth's magnetic field, collectively referred to as strong magnetic fields. Weak magnetic fields, compared to strong magnetic fields, have advantages such as fewer side effects, greater safety, environmental friendliness, and higher efficiency. In recent years, numerous studies have found that weak magnetic field environments (HMF, static magnetic fields <5 μT) can affect tumor occurrence, development, and energy metabolism processes. Static magnetic fields and low-frequency magnetic fields can inhibit the proliferation of various tumors, including leukemia, colon cancer, and breast cancer, as well as the adhesion and migration capabilities of neuroblastoma SH-SY5Y. However, the mechanisms by which magnetic fields regulate tumors remain unknown.

[0004] The magnetic induction hypothesis mainly includes the electromagnetic induction model, the magnetite particle model, the cryptochrome-dependent chemical radical pair model, and the biological compass model. Many animals, such as migratory birds, sea turtles, trout, and butterflies, can use magnetic detection and navigation by sensing information from the Earth's magnetic field. However, most species, especially humans, lack iron-rich tissues / cells and are generally believed to sense magnetic fields through a photochemical compass dependent on cryptochrome (CRY). Foley et al.'s research showed that introducing the human CRY gene could restore magnetic induction in CRY-knockout fruit flies. Summary of the Invention

[0005] To address the problems existing in the prior art, the purpose of this application is to provide the application of the CRY1 gene as a target, to demonstrate that weak magnetic fields can regulate the CRY1 gene and protein in tumor cells, to reveal the magnetic signal transduction process in tumor cells, and to provide a reference for tumor magnetic field therapy, targeted diagnosis and early prevention.

[0006] The technical solution of this application is as follows:

[0007] Applications of the CRY1 gene as a target include:

[0008] Application in the preparation of animal models for studying the regulation of magnetic fields in tumor cells.

[0009] Or its application in the preparation of products in which the magnetic field affects the tumor cells.

[0010] Furthermore, the animal model was constructed by knocking out or overexpressing the CRY1 gene, and the organism's response in the magnetic field environment and the performance of the tumor cells in the magnetic field environment were studied.

[0011] Furthermore, during the research using the animal model, the CRY stabilizer KL001 was used to regulate the body's response or to verify the performance of the tumor cells.

[0012] Furthermore, the weak magnetic field acting on the tumor cells produces effects including at least one of the following:

[0013] Inhibit the transcription of the CRY1 gene in the tumor cells;

[0014] Inhibit the expression of the CRY1 gene in the tumor cells;

[0015] Reduce the content of CRY1 protein in the tumor cells;

[0016] Reduce the activity of the CRY1 protein in the tumor cells.

[0017] Furthermore, the tumor cells include lung cancer cells, colon cancer cells, breast cancer cells, liver cancer cells, squamous cell carcinoma cells, or melanoma cells.

[0018] A product that applies the weak magnetic field described in the above application to the tumor cells, producing an effect including at least one of the following:

[0019] Inhibit the transcription of the CRY1 gene in the tumor cells;

[0020] Inhibit the expression of the CRY1 gene in the tumor cells;

[0021] Reduce the content of CRY1 protein in the tumor cells;

[0022] Reduce the activity of the CRY1 protein in the tumor cells.

[0023] Furthermore, the product is a product that kills tumors and / or inhibits the recurrence and metastasis of said tumors.

[0024] Furthermore, the product can be used in conjunction with formulations or drugs to act on the tumor cells.

[0025] Furthermore, the formulation includes small- to medium-sized molecule radiolabeled tracers.

[0026] Furthermore, the drug includes at least one of chemotherapy drugs, polysaccharide drugs, nucleic acid drugs, peptide or protein drugs.

[0027] Furthermore, the product functions include at least one of the following: early prevention of tumors, screening of chemotherapy drugs, killing the tumor, reducing the proliferation of the tumor, and inhibiting / improving the invasion and metastasis of the tumor.

[0028] This application demonstrates that weak magnetic fields can regulate the CRY1 gene and protein in tumor cells, and that tumor cells can sense changes in magnetic fields through CRY1. In a weak magnetic field environment, CRY1 expression in tumor cells decreases, and preventing CRY1 degradation / overexpression restores the tumor cell proliferation and G0 / G1 cell cycle arrest inhibited by the magnetic field. The weak magnetic field environment significantly inhibits tumor cell proliferation by reducing CRY1 expression, revealing CRY1 as a key regulator of magnetic field sensing and a novel potential target for magnetic field therapy of tumors, as well as its potential role in inhibiting tumor proliferation, invasion, metastasis, and overall tumor treatment in magnetic field therapy.

[0029] The product of this application can also be used as a target for CRY1 gene, CRY1 protein, or CRY1 mRNA in screening or developing drugs for killing tumors and / or inhibiting tumor recurrence and metastasis. Attached Figure Description

[0030] Figure 1 It is a weak magnetic cell culture incubator. Among its components: Figure 1 A is a schematic diagram of a weak magnetic cell culture incubator; Figure 1 B is a picture of the actual weak magnetic cell culture incubator; Figure 1 C is a schematic diagram of a magnetically shielded cell culture box (the control group's geomagnetic field cells are on the steel frame on the upper layer of the magnetically shielded box); Figure 1 D represents the static magnetic field strength distribution inside the cell culture magnetic shielding box (<15nT).

[0031] Figure 2 The HMF environment obtained in Example 2 inhibited the proliferation of various tumor cells. Among them: Figure 2 A- Figure 2 H represents the effect of HMF on the proliferation of tumor cells A431, HCT116, MCF-7, SK-MEL-5, NCI-H460, SK-Hep-1, B16F10 and normal cells HaCaT at different time points.

[0032] Figure 3 In Example 3, HMF inhibited the expression of CRY1 and CRY2 proteins in tumor cells. Wherein: Figure 3 A represents the effect of HMF treatment on CRY protein expression in A431 cells after 3, 5, and 7 days. Figure 3B represents the effect of HMF treatment on CRY protein expression in SK-MEL-5 cells after 3, 5, and 7 days. Figure 3 C represents the effect of HMF treatment on CRY protein expression in B16F10 cells after 3, 5, and 7 days in the presence of CRY stabilizer (KL001). Figure 3 D represents the effect of HMF treatment on the relative expression level of CRY protein in NCI-H460 cells after 3, 5, and 7 days in the presence of CRY stabilizer (KL001).

[0033] Figure 4 This refers to Example 4, which examines the effect of adding the CRY stabilizer KL001 to HMF on the proliferation of tumor cells. Wherein: Figure 4 A- Figure 4 B represents the effect of KL001 on the proliferation ability of HCT116 cells in the HMF environment; Figure 4 C- Figure 4 D represents the effect of KL001 on the proliferation ability of NCI-H460 cells in the HMF environment; Figure 4 E- Figure 4 F represents the effect of KL001 on the proliferation ability of B16F10 cells in the HMF environment; Figure 4 G- Figure 4 H represents the effect of KL001 on the proliferation ability of A431 cells in the HMF environment.

[0034] Figure 5 This is a diagram illustrating the effects of CRY stabilizers in the HMF environment on tumor cell cycle-related proteins (Cyclin A2, Cyclin E2, CDK6) and cell cycle (G0 / G1, S, G2 / M) in Example 5. Wherein: Figure 5 Effects of HMF treatment on the expression of cell cycle-related proteins (Cyclin A2, Cyclin E2, CDK6) in B16F10 cells after 5 days in the presence of KL001; Figure 5 B represents the effect of HMF treatment on the expression of cell cycle-related proteins (Cyclin A2, Cyclin E2, CDK6) in NCI-H460 cells after 5 days in the presence of KL001. Figure 5 C- Figure 5 D represents the effect of HMF treatment on the cell cycle ratio (G0 / G1, S, G2 / M) of B16F10 cells after 5 days in the presence of KL001. Figure 5 E- Figure 5 Effect of HMF treatment on the cell cycle (G0 / G1, S, G2 / M) ratio of NCI-H460 cells after 5 days in the presence of KL001 (F).

[0035] Figure 6 This is a diagram illustrating the effect of HMF on tumor cell proliferation after CRY1 overexpression, as shown in Example 6. Wherein: Figure 6 A shows the expression of CRY1 and CRY2 in tumor cells in GMF and HMF after B16F10 cells overexpress CRY1. Figure 6 B represents the change in the proliferation curve after B16F10 overexpression of CRY1 in the HMF environment; Figure 6 C represents the expression of CRY1 and CRY2 in tumor cells of the GMF and HMF groups after overexpression of CRY1 in NCI-H460 cells; Figure 6 D represents the change in the proliferation curve after NCI-H460 overexpression of CRY1 in the HMF environment; Figure 6 E represents the effect of HMF treatment on the expression of cell cycle-related proteins (Cyclin A2, Cyclin E2, CDK6) after overexpression of CRY1 in B16F10 cells for 5 days. Figure 6 F represents the effect of HMF treatment on the expression of cell cycle-related proteins (Cyclin A2, Cyclin E2, CDK6) in NCI-H460 cells after overexpression of CRY1 for 5 days. Detailed Implementation

[0036] The preferred embodiments of this application will be described in detail below with reference to examples. It should be understood that the following examples are given for illustrative purposes only and are not intended to limit the scope of this application.

[0037] The application of CRY1 gene as a target includes its use in preparing animal models for the study of magnetic field regulation of tumor cells. In the prior art, magnetic field therapy is used as a non-invasive method to inhibit tumors, but the specific response or metabolic pathways are unknown, which will pose difficulties in the study of magnetic field regulation of tumor cells. This application proposes tumor-specific CRY1 overexpression and CRY1 knockout animal models as magnetic field tumor therapy models.

[0038] The application of the CRY1 gene as a target also includes its use in the preparation of products that utilize magnetic fields to influence tumor cells. A weak magnetic field (static magnetic field strength |B|≤5μT) acting on tumor cells produces effects including at least one of the following:

[0039] Inhibits the transcription of the CRY1 gene in tumor cells;

[0040] Inhibits the expression of the CRY1 gene in tumor cells;

[0041] Reduce the level of CRY1 protein in tumor cells;

[0042] Reduces the activity of CRY1 protein in tumor cells.

[0043] Example 1

[0044] Cell culture under extremely weak magnetic environment

[0045] Extremely weak magnetic environment. For example... Figure 1 As shown, the cell culture magnetic shielding box consists of permalloy, a triaxial Helmholtz coil, and an aluminum layer magnetic shielding box. The permalloy and triaxial Helmholtz coil are primarily used to shield static and low- to mid-frequency magnetic fields, while the aluminum layer is designed to shield high-frequency magnetic fields. The static magnetic field strength within the magnetic shielding box is below 15 nT. The residual magnetic field distribution within the magnetic shielding box is relatively uniform. The surface of the magnetic shielding box has sufficient pores to allow cells cultured within it to complete adequate gas exchange and to be cultured in a constant temperature and humidity environment (similar to cells cultured in a geomagnetic field environment). The magnetic shielding box is placed in a regular cell culture incubator to ensure that the cells are under optimal cell culture conditions (95% relative humidity, 5% CO2, 37°C). GMF control cells are cultured on a stainless steel rack at the top of the magnetic shielding box in the same cell culture incubator (Thermo Fisher Scientific), with a local static magnetic field of approximately 50 μT (i.e., GMF).

[0046] Example 2

[0047] HMF inhibition experiment on tumor cell proliferation

[0048] Cell lines: human squamous cell carcinoma A431; human colon cancer cell line HCT116; human breast cancer cell line MCF-7; human lung cancer cell line NCI-H460; human liver cancer cell line SK-HEP-1; melanoma cell lines SK-MEL-5 and B16F10; and human immortalized keratinocytes HaCaT were all derived from the Shanghai Cell Bank.

[0049] Experimental method: CCK-8 assay. CCK-8 can be reduced by dehydrogenases in cell mitochondria to produce a highly water-soluble orange-yellow formazan product. The intensity of its color is directly proportional to cell proliferation and inversely proportional to cytotoxicity. The OD value is measured at a wavelength of 405 nm using an ELISA reader to indirectly reflect the number of viable cells.

[0050] The specific method is as follows:

[0051] Tumor cells in the logarithmic growth phase were seeded into 96-well plates, with 6 parallel wells per group. Cells (600 cells / well, 270 μL of culture medium) were seeded into each well and incubated overnight. Subsequently, they were cultured for different numbers of days (1 day, 3 days, 5 days, and 7 days) under GMF or HMF conditions. 30 μL of CCK8 solution was added to each well, and the plates were incubated at 37°C for 2 hours. The absorbance (OD value) of each well was measured at 405 nm using a microplate reader (Bio-Rad Laboratories).

[0052] The experimental results of HMF inhibiting tumor cell proliferation showed that:

[0053] like Figure 2 A- Figure 2 As shown in Figure H, after 3, 5, and 7 days of HMF treatment, the proliferation capacity of tumor cells A431 (human squamous cell carcinoma cells), HCT116 (human colon cancer cells), MCF-7 (human breast cancer cells), SK-MEL-5 (human melanoma cells), NCI-H460 (human lung cancer cells), SK-Hep-1 (human liver cancer cells), and B16F10 (mouse melanoma cells) was lower than that of the GMF group. After 7 days of HMF environmental treatment, the maximum proliferation inhibition rate of tumor cells A431, HCT116, MCF-7, SK-MEL-5, NCI-H460, SK-Hep-1, and B16F10 decreased by 14.09%, 15.15%, 16.41%, 21.37%, 22.57%, 14.02%, and 24.62% respectively compared to the geomagnetic field. Meanwhile, the proliferation capacity of rapidly proliferating normal human keratinocytes (HaCaT) in the HMF group was comparable to that in the GMF group. In other words, the HMF environment can significantly inhibit the proliferation of tumor cells such as squamous cell carcinoma, colon cancer, breast cancer, melanoma, lung cancer, and liver cancer, while having no significant effect on the proliferation of normal cells.

[0054] Example 3

[0055] Experiment on the effect of HMF on CRY protein expression in tumor cells

[0056] The specific experimental method is as follows:

[0057] Immunoblot assay. Cells in logarithmic growth phase were seeded into medium-sized dishes and incubated overnight. The cells were then cultured in GMF or HMF for a period of time. Tumor cells in logarithmic growth phase were digested with trypsin, collected, washed with PBS, lysed on ice with NP-40 lysis buffer, and centrifuged (12000 rpm, 15 min). The supernatant was collected, and protein concentration was determined using a BCA protein assay kit. Protein samples were separated by SDS-PAGE, transferred to a PVDF membrane, and blocked with 5% skim milk. The membrane was incubated with specific primary antibodies against relevant proteins (CRY1, CRY2, GAPDH, etc.), followed by incubation with rabbit secondary antibody IgG-HRP or mouse secondary antibody IgG-HRP, and then developed using an ECL chemiluminescence assay kit.

[0058] Immunoblot analysis was used to detect the expression of CRY1 and CRY2 proteins in tumor cells by HMF, such as... Figure 3 As shown, compared with the control group GMF, HMF significantly reduced the expression of CRY1 and CRY2 proteins in tumor cells A431 and SK-MEL-5 in a time-dependent manner. The addition of 8 μM of the CRY stabilizer KL001 reversed the HMF-induced degradation of CRY1 and CRY2 in B16F10 and NCI-H460 cells.

[0059] Example 4

[0060] Experimental study on the effect of CRY1 on tumor cell proliferation in HMF

[0061] The specific experimental methods were colony formation experiment and CCK8 proliferation experiment.

[0062] The specific methods for colony formation experiments are as follows:

[0063] Tumor cells in logarithmic growth phase were harvested and their density adjusted to 500-1000 cells / well. The cells were seeded into 12-well plates and cultured overnight at 37°C and 5% CO2. After treatment with or without 8 μM KL001, the cells were cultured in GMF or HMF for 10-14 days. The culture medium was discarded, and the cells were washed three times with PBS. Cells were fixed with 800 μL methanol for 15 min, the methanol was discarded, and the cells were washed three times with PBS. The cells were stained with 0.1% ammonium oxalate-crystal violet solution for 30 min. After washing with PBS and air-drying, the cell colonies were photographed.

[0064] The specific method for the CCK8 proliferation experiment is as follows:

[0065] Tumor cells in logarithmic growth phase were seeded into 96-well plates, with 6 parallel wells per group. Cells (600 cells / well, 270 μL of culture medium) were seeded into each well and incubated overnight. They were then treated with 8 μM KL001 and cultured for different numbers of days (1 day, 3 days, 5 days, and 7 days) under GMF or HMF conditions. 30 μL / well of CCK8 solution was added, and the plates were incubated at 37°C for 2 hours. The absorbance (OD value) of each well was measured at 405 nm using a microplate reader.

[0066] The effects of the CRY stabilizer KL001 on tumor cell proliferation were detected using CCK8 and colony formation assays. Figure 4 As shown, in the presence of KL001, the proliferation of tumor cells HCT116, NCI-H460, B16F10, and A431 in HMF was only slightly altered compared to the GMF group. Specifically, the maximum proliferation inhibition rates of tumor cells B16F10 and NCI-460 in HMF increased by only 8.67% and 8.82% respectively after the addition of KL001. Colony assays showed no significant difference in the number and size of tumor cell colonies after the addition of KL001 to HMF compared to the GMF group. This indicates that the inhibition of tumor cell proliferation by HMF can be offset by the CRY1 stabilizer.

[0067] Example 5

[0068] Flow cytometry detection of the effect of HMF on tumor cell cycle

[0069] The specific experimental method is as follows:

[0070] Cells in the logarithmic growth phase were seeded into 6-well plates and incubated overnight. After culturing in GMF or HMF for a period of time, cells were collected, washed with PBS, fixed overnight with 75% ice-cold ethanol, and centrifuged (3000 rpm, 3 min). 50 μg / mL propidium iodide solution was added, and the cells were incubated at 37°C for 60 min, then centrifuged and the supernatant discarded. Cells were washed with 1% BSADPBS, and cell samples were collected; stored at 4°C, and analyzed using flow cytometry (excitation wavelength 488 nm).

[0071] Flow cytometry and Western blotting were used to detect the effects of adding the CRY1 stabilizer KL001 on tumor cell cycle-related proteins (Cyclin A2, Cyclin E2, CDK6) and cell cycle ratios (G0 / G1, S, G2 / M), such as... Figure 5 As shown, after 5 days of HMF induction in B16F10 and NCI-H460 cells, the expression levels of cell cycle-related proteins Cyclin A2, Cyclin E2, and CDK6 were significantly decreased compared to the GMF group. However, after adding KL001 to prevent CRY1 degradation, the expression levels of Cyclin A2, Cyclin E2, and CDK6 in B16F10 and NCI-H460 cells induced by HMF exposure only slightly decreased. In the presence of KL001, the cell cycle ratio of B16F10 and NCI-H460 cells in the G0 / G1 phase increased by only 5.42% and 8.40% respectively in the HMF group, which was significantly lower than that in the untreated group. The results indicate that preventing CRY1 degradation significantly reduced the cell cycle arrest effect induced by HMF in tumor cells.

[0072] Example 6

[0073] Experiment on the effect of HMF on tumor cell proliferation after CRY1 overexpression

[0074] The specific experimental method for overexpressing CRY1 is as follows:

[0075] For CRY1 overexpression, lentivirus was transfected into cells using HitransG A / P transfection reagent. Cells were cultured for approximately 12 hours, then the medium was replaced with fresh medium. After incubation for 72 hours, fresh medium containing the appropriate concentration of puromycin was added to select successfully transfected cells. The puromycin selection process continued for 14 days, with the medium changed every two days. Afterward, transfected cells were cultured in fresh medium without puromycin. Western blotting was then used to confirm CRY1 overexpression.

[0076] Immunoblotting was used to detect the effect of HMF on cell proliferation after tumor cells overexpressed CRY1, such as... Figure 6As shown, overexpression of CRY1 in B16F10 and NCI-H460 tumor cells significantly enhanced their proliferation in a weak magnetic environment. Furthermore, a slight increase in B16F10 and NCI-H460 cell proliferation was observed in the GMF group after CRY1 overexpression. Five days after HMF induction, the expression levels of cell cycle-related proteins Cyclin A2, Cyclin E2, and CDK6 in B16F10 and NCI-H460 cells significantly decreased. Further investigation revealed that when B16F10 and NCI-H460 cells overexpressed CRY1, the expression levels of Cyclin A2, Cyclin E2, and CDK6 in these cells only slightly decreased after five days of HMF induction. This indicates that HMF can regulate tumor cell proliferation through CRY1 overexpression.

[0077] Based on the above experimental results and analysis, this embodiment demonstrates that tumor cells can sense changes in magnetic fields through CRY1; and that a weak magnetic field environment can regulate tumor cell proliferation through CRY1. This indicates that inhibiting CRY1 expression during tumor treatment can selectively kill tumor cells.

[0078] In summary, this study provides compelling evidence that CRY1 is a key regulator of magnetic field sensing and a novel potential target for magnetic field therapy in tumors. Inhibiting CRY1 expression can effectively suppress tumor cell proliferation, development, invasion, and metastasis, thereby prolonging patient survival. Downregulation of CRY1 expression in tumor cells can significantly improve the quality of life of cancer patients and selectively kill tumor cells, thus improving their survival index. This provides further evidence for the important link between magnetic fields and cancer treatment.

[0079] While specific embodiments are provided in this application, it should be understood that further modifications can be made to this application. Various modifications to these embodiments will be readily apparent to those skilled in the art, and the general principles defined herein may be implemented in other embodiments without departing from the spirit or scope of this application. Therefore, all such modifications or improvements made without departing from the spirit of this application fall within the scope of protection claimed herein.

Claims

1. The application of the CRY1 gene as a target, characterized in that, include: Application in the preparation of animal models for studying the regulation of magnetic fields in tumor cells. Or its application in the preparation of products in which the magnetic field affects the tumor cells.

2. The application according to claim 1, characterized in that, The animal model was constructed by knocking out or overexpressing the CRY1 gene, and the organism's response in the magnetic field environment and the performance of the tumor cells in the magnetic field environment were studied.

3. The application according to claim 1 or 2, characterized in that, During the study using the animal model, the CRY stabilizer KL001 was used to regulate the body's response or to verify the performance of the tumor cells.

4. The application according to claim 1, characterized in that, The effects of a weak magnetic field acting on the tumor cells include at least one of the following: Inhibit the transcription of the CRY1 gene in the tumor cells; Inhibit the expression of the CRY1 gene in the tumor cells; Reduce the content of CRY1 protein in the tumor cells; Reduce the activity of the CRY1 protein in the tumor cells.

5. The application according to claim 1, characterized in that, The tumor cells include lung cancer cells, colon cancer cells, breast cancer cells, liver cancer cells, squamous cell carcinoma cells, or melanoma cells.

6. A product characterized in that, It applies the weak magnetic field described in claim 1 to the tumor cells, producing an effect including at least one of the following: Inhibit the transcription of the CRY1 gene in the tumor cells; Inhibit the expression of the CRY1 gene in the tumor cells; Reduce the content of CRY1 protein in the tumor cells; Reduce the activity of the CRY1 protein in the tumor cells.

7. The product according to claim 6, characterized in that, It can be used in conjunction with formulations or drugs to act on the tumor cells.

8. The product according to claim 7, characterized in that, The formulation includes medium and small molecule radiolabeled tracers.

9. The product according to claim 7, characterized in that, The drug includes at least one of chemotherapy drugs, polysaccharide drugs, nucleic acid drugs, peptide or protein drugs.

10. The product according to claim 6, characterized in that, Its functions include at least one of the following: early prevention of tumors, screening of chemotherapy drugs, killing of tumors, reducing tumor proliferation, and inhibiting / improving tumor invasion and metastasis.

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