KR20130051361A - Composition comprising extract of hwanggeumchal sorghum for the preventing or treating cancer - Google Patents

Abstract

PURPOSE: A composition containing a Sorghum bicolor Moench extract for preventing and treating cancer is provided to suppress metastasis in metastatic breast cancer. CONSTITUTION: A composition for preventing and treating cancer contains a Sorghum bicolor Moench extract as an active ingredient. The extract is a methanol extract of Sorghum bicolor Moench. The cancer is selected from the group consisting of prostate cancer, ovarian cancer, uterine cervix cancer, skin cancer, melanoma, pancreatic cancer, coloproctitis, kidney cancer, leukemia, non-small cell carcinoma, and lung cancer. A composition for suppressing cancer metastasis inhibits metastasis of breast cancer to a lung tissue.

Description

Composition Comprising extract of Hwanggeumchal sorghum for the Preventing or Treating cancer}

The present invention relates to a composition for the prevention and treatment of cancer diseases comprising the extract of golden wax of water, and more particularly to a composition for the prevention and treatment of breast cancer comprising the golden wax of water extract as an active ingredient.

Cancer or neoplasms are malignant neoplasias that occur anywhere in the body. It is characterized by uncontrolled proliferation of cells and is a growing public health problem with an estimated global new incidence of about 6 million people per year. In most countries, cancer is the second leading cause of death after heart disease. This can occur in any organ of the body, but some areas, such as the breast, larynx, intestine, white blood cells, etc., tend to be more prone to attack than others. Each cancer propagates from one cell that divides at a particular stage, which is freed from its regional confinement, forming a family of cells that grow indefinitely and appear in the form of a tumor.

While normal cells are metastasized to tumor cells, significant and hereditary changes occur that allow tumor cells to determine their independent activity almost independently of the law governing the proliferation of all normal cells in the organism. This newly acquired property, known as autonomy, is one of the most important features of tumor cells, since it is not a tumor without such features. Another distinguishing feature of tumor cells is their lack of perfect form.

The difference between cancer cells and normal cells is that cancer cells have a) low pH b) greater free radical properties compared to normal cells c) tumor-producing hormone peptides d) tumor-associated antigens e) lower calcium ions and higher potassium ion concentrations f A) various potassium isotope ratios g) elevated amounts of methylated nucleotides h) higher plasma microprotein and mucopolysaccharide concentrations i) higher need for exogenous zinc and j) higher bio- water content.

Many epidemiological causes of cancer, such as occupational exposure to diet, the environment, certain chemicals or electromagnetic radiation forms, have been found in epidemiological studies. Thus, wherever possible in modern industrial societies, these causes need to be identified and removed from the environment. In reference to the Therapeutic Yearbook, the quest to conquer the dynasty of cancer has always fascinated largely all sectors of science, especially natural chemists. In the nineteenth and twentieth centuries, not only did a lot of research be conducted to determine the driving force behind this fearful disease, but a number of drugs were introduced to counter this threat.

On the other hand, breast cancer, a genetically heterogeneous disease, is the most common malignant disease in women. Around 800,000 new cases are reported worldwide each year (Parkin DM, et al., (1999). CA Cancer J Clin 49: 33-64), and mastectomy is still the best option for medical treatment. Even if the primary tumor is removed surgically, there is a possibility of recurrence at local or distant sites due to micrometastasis that is difficult to detect at diagnosis (Saphner T, et al., (1996). J Clin Oncol, 14, 2738-46). Cytotoxic agents are usually administered as adjuvant therapy after surgery in order to kill these remaining cells or precancerous cells. Traditional chemotherapy is often based on experience or is largely based on histological carcinogenic factors. In the absence of specific epidemiological knowledge, target-oriented therapies are being used in the treatment of breast cancer. Tamoxifen and aromatase inhibitors are representative of these target-oriented therapies and have been reported to be effective when used as adjuvant or chemopreventive in patients with metastatic breast cancer (Fisher B, et al., (1998) J Natl Cancer Inst, 90, 1371-88; Cuzick J (2002) Lancet 360, 817-824).

However, this therapeutic agent has the drawback that it does not show drug sensitivity only in patients expressing estrogen receptors.

In addition, there have been recent reports on side effects such as endometrial cancer and fractures following aromatase treatment in long-term tamoxifen in postmenopausal women (Coleman RE (2004). Oncology. 18 (5 Suppl 3), 16- 20).

As a related prior patent, Korean Patent Publication No. 1020040072646 relates to a herbal medicine composition for cancer treatment, and has anticancer activity against breast cancer, cervical cancer, neuroblastoma, colon cancer, liver cancer, lung cancer, oral cancer, ovarian cancer and prostate cancer. A novel synergistic composition of lignans obtained from a plant extract of Cedrus deodra is described, which comprises 9-13% by weight of (-)-matyroresinol, 75-79% % (-)-Wickstromol, 7-11 wt% dibenzylbutyrolactol and 2.6-3 wt% unidentified material; In addition, the synergistic composition of lignans, together with pharmaceutically acceptable carriers, inhibits the growth of various human cancer cell lines selected from breast, cervical, neuroblastoma, colon, liver, lung, oral, ovarian and prostate tissues. It is described as used.

As another related prior patent, Korean Patent Publication No. 1020070103057 relates to 'composition comprising MDA-7 for the treatment of cancer', and to melanoma differentiation-associated gene 7: MDA- in cancer patients. 7) and methods of treating cancer patients, including providing cyclooxygenase 2: COX-2 inhibitors.

The present invention solves the above problems, and the object of the present invention as devised by the above necessity is to provide a novel cancer prevention and treatment composition.

In order to achieve the above object, the present invention provides a composition for the prevention and treatment of cancer comprising the golden waxy water extract as an active ingredient.

In another aspect, the present invention provides a composition for inhibiting cancer metastasis comprising the golden wax water extract as an active ingredient.

In the present invention, the golden brisk is Sorghum bicolor Moench.

In one embodiment of the present invention, the golden waxy water extract is preferably golden waxy water methanol extract, but all solvent extracts showing the desired effect of the present invention among other solvent extracts are also included in the scope of the present invention.

In one embodiment of the invention, the cancer is a cancer selected from the group consisting of breast cancer, prostate cancer, ovarian cancer, cervical cancer, skin cancer, melanoma, pancreatic cancer, colorectal cancer, kidney cancer, leukemia, non-small cell carcinoma and lung cancer It is preferable, but it is more preferable that it is breast cancer, but it is not limited to this.

As used herein, the term "cancer" is defined as the proliferation of cells in which the unique propensity to lose normal control leads to new properties such as uncontrolled growth, lack of differentiation, local tissue invasion and metastasis. Examples thereof include, but are not limited to, breast cancer, prostate cancer, ovarian cancer, cervical cancer, skin cancer, melanoma, pancreatic cancer, colorectal cancer, kidney cancer, leukemia, non-small cell carcinoma and lung cancer.

As used herein, examples of the term “pharmaceutically acceptable carrier” include any standard pharmaceutical carrier, such as phosphate buffered saline solution, water, emulsions such as oil / water or water / oil emulsions, and various types of wetting agents, and the like. have. In addition, the term includes any agent that has been approved by the Korean government officials or presented in the pharmacopeia for use in animals including humans.

As used herein, the term “treatment” includes the prevention of specific diseases or conditions, the alleviation of symptoms associated with a specific disease or condition and / or the prevention or exclusion of such symptoms. "Prevention" is a treatment that is administered to an individual who does not show signs of the disease, or only shows early signs of the disease to reduce the concern of ongoing pathology with respect to the disease.

"Treatment" is a treatment administered to an individual who exhibits pathological signs to reduce or exclude such signs.

A "therapeutically effective amount" of a compound is the amount of extract sufficient to provide a beneficial effect to the individual to whom the extract is to be administered.

As used herein, the term “treat” includes the prevention of a specific disease, disease, or condition, or the alleviation of symptoms associated with a specific disease, disease, or condition and / or the prevention or exclusion of such symptoms. do.

According to one embodiment, the extract of the present invention may be formulated into a pharmaceutical composition by mixing with one or more pharmaceutically acceptable carriers. Such agents can be administered by standard routes. In general, the mixture may be administered by topical, transdermal, oral, rectal or parenteral (eg intravenous, subcutaneous or intramuscular) route.

When orally administering the extract of the present invention, the extract is administered as a liquid, powder, tablet, capsule or lozenge. The extract can be used in admixture with one or more conventional pharmaceutical additives or excipients used in tablets, capsules, lozenges and other orally administrable forms.

When administered parenterally, more preferably by intravenous injection, the extracts of the invention can be mixed with saline solutions and / or conventional IV solutions. In addition, the mixture may be incorporated into a biodegradable polymer that allows for delayed release of the extract,

In one embodiment, the delivery vehicle is implanted in the vicinity of the site where drug delivery is desired, such as a tumor site. Biodegradable polymers suitable for use in the present invention are known to those skilled in the art and are described, for example, in Brem et al., J. Neurosurg. 74: 441-446 (1991).

The dosage of the extract of the present invention depends on the condition to be treated, the specific extract and other clinical factors such as the weight and condition of humans and animals, and the route of administration of the extract. It is to be understood that the present invention has application examples for both human and veterinary use. In one embodiment relating to administration to a human, a dosage of about 0.1 to 300 mg / kg / day, or about 0.5 to 50 mg / kg / day, or about 1 to 10 mg / kg / day is generally sufficient.

In addition to the extracts of the present invention, it is to be understood that the compositions of the present invention may include solubilizers, inert fillers, diluents, excipients and flavoring agents.

Hereinafter, the present invention will be described.

The present invention is the effect of inhibiting the growth of breast tumors and further prevent metastasis to the lung in mice transplanted with MDA-MB 231 breast cancer cells, one of the aggressive cancer cells of humans (xenotransplantation) Molecular medical mechanisms for

As can be seen through the present invention, the golden waxy water extract can be applied as a pharmaceutical composition showing the cancer prevention and treatment effect and the cancer metastasis inhibiting effect.

1 is a diagram showing that golden wax sorghum extract (HSE) inhibits the growth of breast cancer tumors in human breast cancer xenograft mice, where mice are xenograft to human breast cancer for 6 weeks each, per kilogram of body weight. (vehicle) and gastric administration daily at a dose of 10 mg. A is a picture of xenograft tumor site after 6 weeks of administration. The volume was calculated by measuring the size of the tumor daily at the time of administration and B is a graph showing the change of each tumor growth during the administration of HSE. After 6 weeks of administration, tumors were extracted, the tissues were fixed with paraformaldehyde, cut to a thickness of 5 μm, and the sections were stained with hematoxylin and eosin (H & E staining). C, representative of each group in the tissue cross-section (magnification: × 200, scale bar = 200 ㎛), the arrow indicates the area of necrosis. D, the area of the necrotic part in the tumor cross section was divided into each group and represented graphically. Values are mean ± SE (n = 6) after normalization with vehicle (internal control). Asterisks indicate a statistically significant decrease (B) or increase (D) by t-test (* p <0.05, *** p <0.001).
FIG. 2 shows that HSE inhibits STAT5b / IGF-1R and STAT3 / VEGF signaling pathways and HIF-1α related protein expression in human breast cancer xenograft mice. Growth pathways) and immunohistochemical (IHC) analysis of STAT3 / VEGF (angiogenesis pathway) protein expression (A, B). 5 μm tumor tissue slices were treated with specific primary anti-body STAT3, STAT5b, VEGF and IGF1R. It was detected with secondary antibodies, Alexa Fluor 488 (rabbit) and Alexa Fluor 594 (mouse). IHC staining was performed three times (magnification: × 400). The results confirmed a decrease in the expression of STAT5b, IGF-1R, STAT3 and VEGF without changing nuclear levels. A shows the difference in expression level by IHC of STAT5b / IGF-1R and B of STAT3 / VEGF. C, Differences in expression levels of cancer-producing proteins P-STAT5, P-STAT3, P-IGF-1R, VEGF, VEGF-R2 and HIF-1α on breast cancer xenograft. Protein was extracted from the tissue sample and separated by 10% SDS-PAGE (10 ㎍), western blots were performed. β-actin was used as a quantitative control for protein loading. D, relative expression of protein is expressed graphically (density / actin). Data represents the mean and mean ± SEM of at least 3 replicates. Asterisks indicate a statistically significant decrease by t-test (*** p <0.001).
3 shows that compared with other whole grain extracts, HSE suppresses the cell cycle G1 phase and maintains the expression of tumor suppressor proteins and inhibits the growth of MBA-MD 231 breast cancer cells through the control of tumor proteins. As shown, A, MDA-MB 231 human breast cancer cells were measured for cell viability by MTT assay 24 hours after HSE treatment. B, the proteins involved in the Bcl-2, Cyclin D1, Cyclin E, ppRb and PRB cell cycles were reduced by HSE compared to other crop extracts, and the expression of tumor suppressor proteins such as p53, p21 and BRCA1 was maintained. C, cell cycle inhibition was confirmed by flow cytometry. Based on the reduction of proteins involved in the cell cycle in B was confirmed by flow cytometry through FACs. It was confirmed that the G1 phase cell cycle was further disturbed in HSE treated cells. D, various whole grain extracts were treated with 231 cells of MDA-MB (10 µg / ml) to investigate the expression levels of tumor proteins. Protein was extracted from the sample and separated by 10% SDS-PAGE (10 ㎍), western blots were performed. β-actin was used as a quantitative control for protein loading. Data represents the mean and mean ± SEM of at least 3 replicates. Asterisk indicates IC50 value.
4 is a time- and dose-dependent STAT5b / IGF-1R and STAT3 / VEGF signal pathway inhibitory effect of HSE, MDA-MB 231 cells were treated with HSE (10㎍ / ㎖) for a different time. As a result, breast cancer cells inhibited the STAT5b / IGF-1R and STAT3 / VEGF signaling pathways in a time-dependent manner. B, relative expression of protein is expressed graphically (density / actin). C was treated with various concentrations of HSE in MDA-MB 231 cells. As a result, breast cancer cells inhibited the STAT5b / IGF-1R and STAT3 / VEGF signaling pathways in a concentration dependent manner of HSE. D, relative expression of protein is expressed graphically (density / actin). Protein was extracted from the sample and separated by 10% SDS-PAGE (10 ㎍), western blots were performed. β-actin was used as a quantitative control for protein loading. E, HSE (24hr 10 ㎍ / ㎖) treated with RT-PCR analysis of MDA-MB 231 cells showed mRNA regulation of mRNA levels of IGF-1R and VEGF. 18S RNA was used as a control. Data represents the mean and mean ± SEM of at least 3 replicates. Asterisks indicate a statistically significant decrease by ANOVA.
5 is a diagram showing the inhibition of the binding activity of the VEGF promoter region of STAT5b to the IGF-1R and STAT3 of HSE. A, electrophoretic mobility shift assay (EMSA), for the treatment of 24hr HSE in MDA-MB 231 cells Inhibits the DNA binding activity of the binding site from STAT5b to IGF-1R (i) and from STAT3 to VEGF (ii). B, P-STAT5, P-STAT3, VEGF and IGF-1R reduction was confirmed by HSE in the nuclear protein extract (NE) of MDA-MB 231 cells. C and D show that the activity of STAT5b / IGF-1R and STAT3 / VEGF promoters in COS-7 cells is inhibited by treatment of HSE. COS-7 cells were transiently co-transfected with STAT5b / IGF-1R (C) and STAT3 / VEGF (D) genes. Data represents the mean and mean ± SEM of at least 3 replicates. Asterisks indicate a statistically significant decrease by t-test (*** p <0.001).
Figure 6 is a diagram showing the blocking of breast cancer metastasis to the lung by HSE on xenotransplantation animal model, the effect analysis by HSE in lung metastasis experimental animal model. Mice were injected with MDA-MB 231 cells (1 × 10 7). One group of mice (N = 6) was given HSE daily for 30 days and the other group (N = 6) received water using the same schedule. After 6 weeks of administration, the lungs were removed, the tissues were fixed with paraformaldehyde, cut to a thickness of 5 μm, and the sections were stained with hematoxylin and eosin (H & E staining). A, a representative photograph of each group in the tissue cross section (magnification: x 200, scale bar = 200 μm), and the arrow indicates the area of metastasis. B was plotted through quantitative analysis of the transition area, marking areas of metastatic nodules in each section of A. HSE treatment (24hr 10㎍ / ㎖) in C, MDA-MB 231 cells confirmed the inhibitory effect on migration. After 24 hours, no cell movement was observed in the HSE-treated group, but active migration was observed in the control group. Data represents the mean and mean ± SEM of at least 3 replicates. Asterisks indicate a statistically significant decrease by t-test (*** p <0.001).

The present invention will now be described in more detail by way of non-limiting examples. The following examples are intended to illustrate the invention and the scope of the invention is not to be construed as being limited by the following examples.

Example  One: HSE  Produce

Golden wax sorghum was supplied and used by the Rural Development Administration. The sample (50 g) was lyophilized (-40 ° C.), pulverized and homogenized at room temperature, and extracted with 30% 0.1 N HCl (30-40 ° C.). Then, solution filtering (at room temperature, whatman No. 42) was carried out, re-extracted with 100% methanol (30-40 ° C.) and overnight lyophilized (-40 ° C.) to use in the examples below.

Example  2: cell culture

MDA-MB-231 human breast cancer cells were cultured in L-15 medium containing 10% fetal bovine serum (FBS), 2 mM glutamine and 100 U / ml penicillin and streptomycin at 37 ° C., 5% CO 2. In addition, COS-7 monkey kidney cells were cultured in DMEM (Gibco-BRL, USA) containing 10% fetal bovine serum (FBS), 2 mM glutamine and 100 U / ml penicillin and streptomycin at 37 ° C. and 5% CO 2. .

The cultured cells were resuspended in a suitable medium at a density of 2.5 × 10 5 cells / ml every experiment.

Example  3: Animal test results Xenogrft Nude In mice HSE Human breast cancer tumor growth inhibitory effect HSE On by IGF Decreased Expression of -I Genes

In the present invention, the following animal experiment (xenograft) was conducted to investigate the effect of HSE substances on the growth of human breast tumors.

That is, Balb / c mouse species was purchased from an experimental animal production company (Orient Bio Co., Ltd.) and injected with MDA-MB 231 cells, a representative human breast cancer cell line, on both sides for 6 weeks to generate tumors Accordingly measure the size of the tumor. Thereafter, the test was performed using 12 xenografted mice (xenografted mice), which were divided into groups not fed with HSE (control) and fed groups. After HSE, daily tumor size (mm ³ by volumetric formula) was measured.

As a result, after about 30 days, the tumor size stopped growing in the administration group (Fig. 1-b). Among them, the shape and size of tumors of representative animals are shown in comparison with the control group (FIG. 1-a). Next, the human breast tumor was isolated by cervical dislocation and various tumor suppression-related indices in tumor tissues were measured by the following experimental method.

 ① Western blotting

 ② immunohistochemistry

 ③ Histology (H & E staining)

 ④ NE (nuclear protein) measurement

The xenograft mouse tissue was cut into 5 thicknesses and observed by morphological changes by H & E staining. As a result, necrosis, which was not seen in the tumor tissue of the control group, was significantly progressed in the tumor tissue of the HSE treated group (Fig. 1-c, d).

In addition, after attaching STAT5b, STAT3, IGF-1R, and VEGF specific primary antibodies, secondary antibodies (Alexa Fluor 488 (rabbit) and Alexa Fluor 594 (mouse)) were used for detection. STAT5b / IGF-1R specific immunohistochemistry showed that STATb / IGF-1R levels were reduced without nuclear damage (FIG. 2-a). STAT3 / VEGF specific immunohistochemistry showed a decrease in STAT3 / VEGF levels without nuclear damage (Fig. 2-b).

As a result of animal experiments, the proteins of human breast tumor tissues of xenograft nude mice were extracted and the expression levels of pSTAT5, pSTAT3, IGF-1R, VEGF, VEGF-R2 and HIF-1a proteins were reduced by HSE (FIG. 2). -c, d).

Example  4. HSE Study on the viability of cancer cells

To investigate the effect of HSE on the viability of cancer cells, the following experiments were performed.

First, the cancer cell line MDA-MB 231 cells were treated in 96-well plates for 24 hours according to various concentrations of HSE (2.5, 5, 7.5, 10, 12.5 μg), and then cultured only for surviving cells. After treatment with MTT (blue formazan) was incubated for 4 hours at 37 ℃. The cultured cells were disrupted and cell lysate was obtained, and the formazan product was measured at 550 nm after lysis by adding DMSO to each well. The process was repeated three times, and the results are shown in FIG. 3A.

As shown in FIG. 3A, it was confirmed that dose-dependent cell growth was inhibited in the group treated with HSE.

Example  5. HSE Influence of cancer on the cell cycle of cancer cells

In order to determine the effect of HSAE on the cell cycle of cancer cells (MDA-MB 231), the experiment was as follows.

In the case of PI, a substance that binds to the nucleus. When a cell dies severely, a hole is formed in the cell membrane, and the nucleus is exposed to the outside, so that the PI binds. PI can identify the cell cycle in detail. Breast cancer cell line MDA-MB 231 was used to confirm that the cell cycle is inhibited in the G1 phase in Figure-3c.

Example  6: HSE end STATs , IGF - IR   And p53  Investigate the effect on expression of proteins

In order to investigate how it affects the expression of various proteins regulated by HSE, experiments were as follows.

In the present invention, we found that 10 μg HSE reduced the viability of human breast cancer cells, Bcl-2, Cyclin D1, Cyclin E, pRb, STAT5b, STAT3, IGF-1R, VEGF, VEGFR2, JAK2 and phosphorylated pRb. , STAT5b, STAT3, IGF-1R protein expression level was inhibited, whereas the expression level of tumor suppressor proteins such as p53, p21, BRCA1 was confirmed to increase (Fig. 3-b, c).

In addition, TAT5b, STAT3, IGF-1R, VEGF, VEGFR2 proteins, such as p53 is increased while reducing the expression level depending on the treatment time and concentration was confirmed (Fig. 4-a, b, c, d).

Example  7: HSE On by IGF - IR  And VEGF  Investigation of Reduction of Gene Expression

Total RNA Semi-quantitative analysis using RT-PCR was performed to investigate the effects of HGF-stimulated human breast cancer cells (MDA-MB 231 cells) on the transcriptional activity of IGF-1R and VEGF (Figure 4-e). ).

First, the human breast cancer cell line MDA-MB 231 was treated with HSE concentrations (0, 2.5, 5, and 10 µg), and the mRNAs of IGF-1R and VEGF genes cultured for 24 hours were subjected to real-time polymerase chain reaction ( PCR) was performed to measure each.

Each measurement was obtained by repeating the measurement three times by normalizing the β-actin mRNAs level.

As a result, as shown in Figure 4-e, when HSE treatment, it was found that IGF-IR and VEGF gene expression decreased with concentration.

Example  8: STAT5b  Protein and IGF - IR  gene, STAT3  Protein and VEGF  Inhibition of binding site and mutual binding force between genes

Certain stimulants are necessary for STAT5b and STAT3 protein synthesis to occur in the MDA-MB 231 cell line. The synthesized STAT5b protein enters the nucleus and binds to the STAT5 binding site of IGF-IR, indicating its activity, and confirms STAT5 and IGF-IR binding activity, as well as STAT3 and VEGF binding activity. EMSA (electrophoretic mobility shift assay, kit: Panomics, AY2002) was performed.

To determine the effect of HSE, 100 μg of HSE was treated for 24 h. As a result, it was found that the binding force between IGF-IR gene and STAT5b and VEGF and STAT3 were decreased by HSE (FIG. 5A). In addition, the expression of pSTAT5, pSTAT3, VEGF and IGF-1R protein on the nuclear protein was found to be inhibited by HSE (Fig. 5b).

Example  9: HSE On by STAT5b , STAT3 , IGF -1R and VEGF Investigation of promoter activity

To investigate whether the IGF-1R and VEGF promoters are activated by STAT5b and STAT3 proteins, STAT5b / IGF-1R (Dr. Honglin Jiang, Virginia Polytechnic Institute and State University, USA.) And STAT3 / VEGF promoters (Dr. Carrie Shemanko, Department of Biological Sciences, University of Calgary, 2500 University Drive NW, Calgary, AB, T2N 1N4, Canada) were investigated.

Specifically, the activation levels of the STAT5b / IGF-1R and STAT3 / VEGF promoters in HSE treated cells were compared by measuring relative luciferase activity.

As a result, as shown in FIG. 5, it was found that the activities of the STAT5b / IGF-1R and STAT3 / VEGF promoters were reduced by HSE (FIGS. 5-c and d).

Example  10: HSE Induce Metastasis Inhibition in Metastatic Breast Cancer

Animal Experimental Model (xenograft) Balb / c mice were injected with MDA-MB 231 cells, a representative human breast cancer cell line, and then divided into HSE-fed (control) and fed groups. Thirty days after the daily administration of HSE, the lungs were removed from all rats, the tissues were cut into 5 thicknesses, and morphological changes were observed by H & E staining. It was confirmed that not observed in the lung tissue of the group (Fig. 6-a, b).

6-c, MDA-MB 231 cells (10 ⁵ cells / ml) were grown in DMEM medium, and after 24 hours, they were changed to medium with and without HSE.

6-c Ai. Real time cell images (FIG. 6-c Aii) were obtained after 24 hours in MDA-MB 231 cells without HSE. 6-c Aiii. Real-time cell images (6-c AVII) were obtained after 24 hours in MDA-MB 231 cells with 10 μg HSE.

As a result, it was confirmed that in the cells treated with HSE, inhibition of cell migration proceeded differently from the control group.

Claims (8)

Cancer preventive and therapeutic composition comprising the golden wax water extract as an active ingredient. [Claim 2] The composition for preventing and treating cancer according to claim 1, wherein the golden waxy water extract is golden waxy water methanol extract. The method of claim 1,
The cancer is cancer, prostate cancer, ovarian cancer, cervical cancer, skin cancer, melanoma, pancreatic cancer, colorectal cancer, kidney cancer, leukemia, non-small cell carcinoma and lung cancer characterized in that the cancer selected from the group consisting of lung cancer Composition. The method of claim 1,
The cancer is a cancer prevention and treatment composition, characterized in that the breast cancer. Cancer metastasis inhibiting composition comprising the golden shingsu extract as an active ingredient. The composition for inhibiting cancer metastasis according to claim 5, wherein the golden waxy water extract is golden waxy water methanol extract. 6. The method of claim 5,
The cancer is a cancer metastasis inhibiting composition, characterized in that the cancer selected from the group consisting of breast cancer, prostate cancer, ovarian cancer, cervical cancer, skin cancer, melanoma, pancreatic cancer, colorectal cancer, kidney cancer, leukemia, non-small cell carcinoma and lung cancer . 6. The method of claim 5,
The cancer metastasis composition for inhibiting cancer metastasis, characterized in that inhibiting the metastasis of breast cancer to lung tissue.

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