CN112210604A - Application of CAS as triple negative breast cancer marker and application of CAS in inhibiting or treating triple negative breast cancer - Google Patents
Application of CAS as triple negative breast cancer marker and application of CAS in inhibiting or treating triple negative breast cancer Download PDFInfo
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Abstract
The invention belongs to the technical field of biomedicine, and relates to a triple negative breast cancer cell model and an animal model for knocking down a CAS gene and application thereof. According to the invention, the mRNA level of the CAS of a patient with triple negative breast cancer is found to be significantly higher than that of a patient with non-triple negative breast cancer through database mining analysis, then an in-vitro cytological model for knocking down the CAS gene and a nude mouse tumor-bearing animal model are established, the action and mechanism of the CAS gene in triple negative breast cancer cells are researched, and an anti-cancer drug with treatment efficacy on triple negative breast cancer is researched and prepared according to a signal path for controlling the occurrence and development of triple negative breast cancer by CAS. The model provided by the invention can provide a new research method for searching the pathogenesis of triple negative breast cancer.
Description
Technical Field
The invention relates to the technical field of biomedicine, in particular to application of CAS (CAS) as a triple negative breast cancer marker, application of experimental verification of CAS regulation in inhibiting or treating triple negative breast cancer and application of CAS regulation in preparing a medicament for inhibiting triple negative breast cancer.
Background
The breast cancer is one of the most common female malignant tumors, a global cancer statistical data report in 2018 shows that the breast cancer is the female cancer with the highest incidence rate (24.2%), and meanwhile, a latest cancer statistical data report released in 2018 by the cancer center in China shows that the female malignant tumor with the highest incidence rate in China is the breast cancer (17.1%), so that the breast cancer is an important factor seriously threatening the physical health of women.
The breast cancer is a highly heterogeneous malignant tumor, and can be classified into 5 types of Luminal A type (ER and/or PR positive, Her-2 negative), Luminal B type (ER and/or PR positive, Her-2 positive), Her-2 positive (ER and PR negative, Her-2 positive) and Basal like breast cancer (ER negative, PR negative, Her-2 negative, CK5/6 positive, and/or Her-1 positive) and normal breast cancer type according to the immunohistochemical detection result. Among them, we frequently hear Triple Negative Breast Cancer (Triple Negative Breast Cancer) immunostaining results similar to Basal like type, the expressions of ER, PR and Her-2 are all Negative, Triple Negative Breast Cancer and Basal like Breast Cancer are distinguished in that Basal like Breast Cancer is mainly determined by gene chip, Triple Negative Breast Cancer is mainly determined by immunohistochemical staining, and about 80% of Triple Negative Breast Cancer reported in literature is Basal like, and in some cases, the two can be equally combined. The triple negative breast cancer accounts for about 15% of breast cancer, is higher than young women, is the most invasive type of breast cancer, and the tumor of a patient is easy to generate lung metastasis and brain metastasis. Therefore, it is of great significance to find specific targets for treating triple negative breast cancer.
CAS is a nuclear transport factor responsible for the transport of immunoprotein-a from the nucleus to the cytoplasm, and plays a key role in nuclear and cytoplasmic transport of proteins. Although studies have reported that CAS has some correlation with breast cancer occurrence, the specific mechanism of action of CAS in triple negative breast cancer remains unclear. The present study found that CAS expression was significantly higher in patients with triple negative breast cancer than in patients with non-triple negative breast cancer, and that CAS plays a key role in the survival, migration and invasion of triple negative breast cancer cells and tumor growth. At present, the CAS is not reported as a triple negative breast cancer marker.
Disclosure of Invention
The present invention is based on the following findings: expression of CAS in triple negative breast cancer tissues was found to be significantly higher than non-triple negative breast cancer tissues by database mining analysis.
The purpose of the invention is as follows: aiming at the problems or the defects in the prior art, the application of CAS as a triple negative breast cancer marker, the application of experimental verification of CAS regulation in the aspect of inhibiting or treating triple negative breast cancer and the application of CAS regulation in the aspect of preparing a medicine for inhibiting triple negative breast cancer are provided, a new direction is provided for screening, diagnosis, prognosis evaluation and treatment of triple negative breast cancer, and a new research method is provided for searching the pathogenesis of triple negative breast cancer.
To achieve the above object, the embodiments of the present invention provide an application of CAS as a triple negative breast cancer marker.
Further, the CAS is used as a marker in screening, diagnosing and prognosis evaluation reagents of triple negative breast cancer tumors.
Preferably, the kit contains reagents for quantifying CAS mRNA.
The embodiment of the invention also provides an application of experimental verification of CAS regulation in inhibition or treatment of triple negative breast cancer, which is characterized by comprising the following steps:
s1, constructing a CAS knock-down triple negative breast cancer cell model and a CAS knock-down triple negative breast cancer animal model;
s2, carrying out transcriptome sequencing on the CAS-knocked-down triple negative breast cancer cell model through cell viability, cell cloning experiments, cell migration and invasion experiments and a subcutaneous tumor-bearing model, obtaining a significantly changed signal path through KEGG path enrichment, and researching the effects of CAS on regulation and control of proliferation, migration and invasion of triple negative breast cancer cells.
Specifically, in step S1, the method for knocking down a triple negative breast cancer cell model of CAS comprises the following steps: the gene is constructed by knocking down the CAS gene of a triple negative breast cancer cell line MDA-MB-231 by using a lentivirus transfection technology.
Specifically, in step S1, the CAS-knockdown triple negative breast cancer animal model includes the following steps: the three-negative breast cancer cell line with the CAS knock-down function is constructed by using lentivirus and then injecting the cells into nude mice subcutaneously.
Specifically, in step S1, the animal used in the constructed triple negative breast cancer animal model may be a nude mouse or other immunodeficient mouse.
The embodiment of the invention also provides an application of CAS regulation in preparing a medicine for inhibiting triple negative breast cancer, which is characterized in that: according to the signal path of the CAS regulation and control of the occurrence and development of the triple negative breast cancer, the anti-cancer medicine with the treatment effect on the triple negative breast cancer is developed and prepared.
Furthermore, the signal path for the CAS to regulate the occurrence and development of the triple negative breast cancer is obtained by using lentivirus to knock down the CAS in the triple negative breast cancer cell line, then performing transcriptome sequencing, and enriching the CAS into a group of signal paths which are significantly changed before and after the knock-down through a KEGG path.
The technical scheme of the invention has the following beneficial effects:
(1) the application of the CAS of the invention as a triple negative breast cancer marker is based on the biological information database data analysis of the remarkable high expression of the CAS in triple negative breast cancer in breast cancer, so as to discover a new marker of the triple negative breast cancer marker, and the CAS is used as the triple negative breast cancer marker and the application of the CAS in screening, diagnosis and prognosis evaluation of the triple negative breast cancer.
(2) The application of CAS regulation in the aspect of inhibiting or treating triple negative breast cancer is experimentally verified, meanwhile, the CAS of MDA-MB-231 cells is knocked down by using a lentivirus transfection technology, a triple negative breast cancer cell model and an animal model for knocking down the CAS are established, transcriptome sequencing is performed through cell viability, a cell cloning experiment, a cell migration and invasion experiment and a subcutaneous tumor-bearing model at the same time, the effects of CAS regulation on proliferation, migration and invasion of triple negative breast cancer cells are researched, and a new research method is provided for searching the pathogenesis of triple negative breast cancer.
(3) The application of the CAS regulation and control in the preparation of the medicine for inhibiting the triple negative breast cancer provides a new direction for researching and preparing the anti-cancer medicine with the treatment effect on the triple negative breast cancer through the obtained signaling path for the CAS regulation and control of the occurrence and development of the triple negative breast cancer.
Drawings
FIG. 1 is a graph showing the statistical results of CAS expression in non-triple negative breast cancer and triple negative breast cancer according to the present invention;
FIG. 2 is a graph showing the results of the cell viability experiment according to the present invention;
fig. 3 is a graph showing experimental results of cell migration and cell invasion in the present invention, in which fig. 3A and 3B are a graph and a statistical graph of cell migration results, respectively, and fig. 3C and 3D are a graph and a statistical graph of cell invasion results, respectively.
Fig. 4 is a graph of experimental results of a nude mouse tumor-bearing animal model according to the present invention, wherein fig. 4A is a tumor picture (left) and a tumor picture (right) of a tumor under the nude mouse skin, fig. 4B is a growth curve of the tumor, and fig. 4C is a tumor weight statistical chart.
FIG. 5 is a graph of the enrichment results of the KEGG pathway for transcriptome sequencing in the present invention.
Detailed Description
In order to make the technical problems, technical solutions and advantages of the present invention more apparent, the following detailed description is given with reference to the accompanying drawings and specific embodiments.
Example 1
The expression of CAS mRNA in triple negative breast cancer is obviously higher than that in non-triple negative breast cancer tissues
According to the invention, database mining analysis shows that the expression of CAS mRNA in triple negative breast cancer is significantly higher than that in non-triple negative breast cancer tissues, as shown in FIG. 1, the specific experimental steps are as follows: downloading a breast cancer data set from a UCSC Xena database, sorting the data, counting the expression quantity of the CAS gene in triple negative breast cancer and non-triple negative breast cancer, and carrying out result statistical analysis by using Graph prism 8.0.
Example 2
Construction of triple negative breast cancer cell model and animal model for knocking down CAS
In the invention, a triple negative breast cancer cell model and an animal model for knocking down CAS are constructed, and a cell model and an animal model of a triple negative breast cancer line MDA-MB-231 for knocking down CAS are established by utilizing a lentivirus-mediated CAS gene silencing technology.
In the invention, a triple negative breast cancer cell model system MDA-MB-231 cell model for knocking down CAS is constructed, and the specific construction methods are respectively as follows: triple negative breast cancer cell line MDA-MB-231 was expressed at 2X 105And (3) inoculating the cells in a 6-well plate, adding 4uL of lentivirus and a transfection assisting reagent polybrene with the final concentration of 5ug/mL into each well according to the virus use instruction after the cells adhere to the wall next day, adding puromycin after 48 hours, and screening to construct a triple-negative breast cancer cell model for stably knocking down CAS after one week.
In the invention, a triple negative breast cancer animal model MDA-MB-231 nude mouse subcutaneous tumor-bearing animal model for knocking down CAS is constructed, and the specific construction method is as follows: breast cancer cells MDA-MB-231 were treated at 1X 106Inoculating in 20cm ultra-large dish, after the next day of cell adherence, dividing the cells into experimental group and control group, transfecting reagent according to MOI =20 concentration according to lentivirus use instruction, collecting cells after 48h, and re-suspending to 1 × 106Per 100uL of cell suspension, while adding polybrene to a final concentration of 5ug/mL, the cell suspension was placed on ice and the suspension was processed in the animal house at 1X 106Injecting the concentration of 100uL into the subcutaneous of a mouse, and establishing a subcutaneous tumor-bearing animal model of the nude mouse.
Example 3
Cell viability assay, cell migration and invasion assay
1. Cell viability assay comprising the steps of:
(1-1) the above cell model was seeded at a density of 2000 cells/well in a culture plate at 37 ℃ with 5% CO2 After 24 hours of culture in an incubator, CCK8 working solution and CO are added2 The box was incubated for 2 hours;
(1-2) detecting the OD value by a microplate reader, comparing the vitality condition of the cells, and detecting the vitality of the cells every other day until the vitality experiment of the cells is completed.
As shown in fig. 2, compared with the blank control group, the activity of the triple-negative breast cancer cells in the CAS-knockdown experimental group is significantly less than that in the blank control group, and it can be seen that the knockdown CAS significantly inhibits the activity of the triple-negative breast cancer cells.
2. Cell migration and invasion assay comprising the steps of:
(2-1) the Cell model with serum-free medium heavy suspension, to a certain number of cells in Corning Cell Culture Insert (Transparent PET Membrane 24 Well 8.0 um pore size)/Corning Matrigel Matrix Transwell, 24-hole plate lower chamber with 10% FBS medium;
(2-2) standing at 37 ℃ with 5% CO2After 24 hours incubation in the incubator, 4% PFA was fixed for 10 minutes, washed twice with PBS, stained with hematoxylin for 10 minutes, cells inside the Insert/Transwell were wiped off with a cotton swab, photographed under a microscope and counted for the number of cells passing through the Insert/Transwell, completing the cell migration and invasion experiments.
The experimental results are shown in fig. 3, and the results of the cell migration and invasion experiments are shown in a graph, and the data show that knocking down the CAS significantly weakens the migration and invasion capacity of the triple negative breast cancer cells. From the cell migration result graphs and the statistical graphs of fig. 3A and 3B, it can be seen that the migration ability of the experimental group of triple negative breast cancer cells after CAS knockdown is significantly weakened compared to the blank control group; from the cell invasion result graphs and the statistical graphs of fig. 3C and 3D, it can be seen that the invasion capacity of the experimental group of triple negative breast cancer cells after CAS knockdown is significantly weakened compared to the blank control group.
Example 4
Construction of CAS knock-down breast cancer subcutaneous tumor animal model
The construction method of the breast cancer subcutaneous tumor animal model for knocking down CAS comprises the following steps: breast cancer cells MDA-MB-231 were treated at 1X 106The seeds are planted in a 20cm ultra-large dish,the following day after cell attachment, the cells were divided into experimental and control groups, transfected according to MOI =20 concentration according to lentivirus instructions, harvested after 48h and resuspended to 1 × 106Per 100uL of cell suspension, while adding polybrene to a final concentration of 5ug/mL, the cell suspension was placed on ice and brought into the animal house, and the cell suspension was mixed at 1X 106Per 100uL of the tumor volume and weight were measured every other day until the tumor volume reached the animal ethical limit of 1500 mm3Mice were sacrificed, tumors removed, photographed and tumor volume and weight recorded for statistical analysis with Graph prism 8.0.
The results are shown in the experimental result diagram of the nude mouse tumor-bearing animal model in fig. 4, and it can be seen that fig. 4A is a tumor image (left) and a tumor image (right) of a tumor under the nude mouse skin, and it can be seen from the left image in fig. 4A that compared with the experimental group of the breast cancer subcutaneous tumor animal model with CAS knock-down, the tumor volume taken out by the experimental group is significantly smaller than that taken out by the blank control group; from the growth graph of the tumor of fig. 4B, it can be seen that the tumor growth rate of the CAS-knockdown experimental group was significantly lower than that of the blank control group; from the tumor weight statistical plot of fig. 4C, it can be seen that the tumor weight taken out of the experimental group was significantly less than that of the blank control group.
Example 5
KEGG enrichment pathway following transcriptome sequencing (RNA-seq) for CAS-knockdown triple negative breast cancer cell models
A method of obtaining a KEGG enrichment pathway comprising the steps of: collecting a control group cell line MDA-MB-231-LV-U6 and an experimental group cell line MDA-MB-231-shCAS 6 days after CAS knock-down, storing the samples in a TRIZOL refrigerator at-80 ℃, extracting total RNA for quality detection, selecting a sample with 260/280 of 1.8-2.0 and agarose gel electrophoresis detection of 28S:18S at least greater than 1.8, sending the sample to a sequencing company, constructing a library by the sequencing company, performing on-machine sequencing and other steps, sending obtained sequencing data back after sequencing is completed, and performing interpretation and subsequent analysis.
Results as shown in fig. 5, analysis of the transcriptome sequencing data showed: after knockdown of CAS, there are more signal pathways that change significantly, with higher significance including: lysosome, State cancer, Dorso-viral axis formation, Focal addition, TNF signaling pathway, and the like.
The invention discovers that the cell activity, the proliferation capacity, the migration capacity and the invasion capacity of the triple negative breast cancer cell MDA-MB-231 with the CAS knocked down are obviously weakened; knockdown CAS lentiviral interference inhibited the growth of triple negative breast tumors in a CAS-knockdown triple negative breast cancer mouse subcutaneous tumor-bearing model. Meanwhile, transcriptome sequencing is carried out on a triple negative breast cancer cell MDA-MB-231 cell model with CAS knock-down, and a significantly changed signal pathway is obtained through KEGG pathway enrichment; therefore, the preparation method can be used for developing and preparing the anti-cancer drug with the treatment effect on the triple negative breast cancer, and a new direction is provided for developing the anti-cancer drug for the triple negative breast cancer.
While the foregoing is directed to the preferred embodiment of the present invention, it will be understood by those skilled in the art that various changes and modifications may be made without departing from the spirit and scope of the invention as defined in the appended claims.
Claims (9)
- The application of CAS as a triple negative breast cancer marker.
- 2. The use of CAS according to claim 1 as a marker for triple negative breast cancer, wherein: the CAS is used as a marker in screening, diagnosing and prognosis evaluation reagents of triple negative breast cancer tumors.
- 3. The use of CAS as a marker for triple negative breast cancer according to claim 2, wherein said kit is a reagent containing quantitative CAS mRNA.
- 4. Experimentally verifying the application of CAS regulation in inhibiting or treating triple negative breast cancer, the method is characterized by comprising the following steps:s1, constructing a CAS knock-down triple negative breast cancer cell model and a CAS knock-down triple negative breast cancer animal model;s2, carrying out transcriptome sequencing on the CAS-knocked-down triple negative breast cancer cell model through cell viability, cell cloning experiments, cell migration and invasion experiments and a subcutaneous tumor-bearing model, obtaining a significantly changed signal path through KEGG path enrichment, and researching the effects of CAS on regulation and control of proliferation, migration and invasion of triple negative breast cancer cells.
- 5. The experimental validation of the use of CAS modulation for the inhibition or treatment of triple negative breast cancer according to claim 4, wherein said step S1 knockdown of the triple negative breast cancer cell model for CAS comprises the following steps: the gene is constructed by knocking down the CAS gene of a triple negative breast cancer cell line MDA-MB-231 by using a lentivirus transfection technology.
- 6. The experimental validation of the CAS modulation for use in inhibiting or treating triple negative breast cancer according to claim 4, wherein the step S1 of knocking down the triple negative breast cancer animal model of CAS comprises the following steps: the three-negative breast cancer cell line with the CAS knock-down function is constructed by using lentivirus and then injecting the cells into nude mice subcutaneously.
- 7. The experimental verification of the CAS regulation for inhibiting or treating triple negative breast cancer as claimed in claim 4, wherein the animal used in the triple negative breast cancer animal model constructed in step S1 can be nude mouse or other immune deficient mouse breed.
- The application of CAS regulation and control in the preparation of drugs for inhibiting triple negative breast cancer is characterized in that: according to the signal path of the CAS regulation and control of the occurrence and development of the triple negative breast cancer, the anti-cancer medicine with the treatment effect on the triple negative breast cancer is developed and prepared.
- 9. The application of the CAS regulation in preparing a drug for inhibiting triple negative breast cancer according to claim 8, wherein the signaling pathway for the CAS regulation of the occurrence and development of triple negative breast cancer is obtained by using lentivirus to knock down CAS in a triple negative breast cancer cell line, then performing transcriptome sequencing, and enriching a group of signaling pathways which are significantly changed before and after the knock-down through a KEGG pathway.
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Citations (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN110747170A (en) * | 2019-11-18 | 2020-02-04 | 南通大学 | Breast cancer cell model with CAS knock-down and cytological experiment using same |
| CN111424090A (en) * | 2020-04-20 | 2020-07-17 | 中国科学院昆明动物研究所 | Application of SGCE gene as triple negative breast cancer marker |
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| Publication number | Priority date | Publication date | Assignee | Title |
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| CN110747170A (en) * | 2019-11-18 | 2020-02-04 | 南通大学 | Breast cancer cell model with CAS knock-down and cytological experiment using same |
| CN111424090A (en) * | 2020-04-20 | 2020-07-17 | 中国科学院昆明动物研究所 | Application of SGCE gene as triple negative breast cancer marker |
Non-Patent Citations (2)
| Title |
|---|
| CHING-FONG LIAO等: "CSE1L/CAS, the cellular apoptosis susceptibility protein, enhances invasion and metastasis but not proliferation of cancer cells", JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH, vol. 27 * |
| MEI YE等: "Cellular apoptosis susceptibility protein (CAS) suppresses the proliferation of breast cancer cells by upregulated cyp24a1", MEDICAL ONCOLOGY, vol. 37 * |
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