CN113134077A - Application of efficient transcription factor KLF4 in regulation and control of colorectal cancer metastasis - Google Patents
Application of efficient transcription factor KLF4 in regulation and control of colorectal cancer metastasis Download PDFInfo
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K38/00—Medicinal preparations containing peptides
- A61K38/16—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof
- A61K38/17—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans
- A61K38/1703—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans from vertebrates
- A61K38/1709—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans from vertebrates from mammals
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P35/00—Antineoplastic agents
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P35/00—Antineoplastic agents
- A61P35/04—Antineoplastic agents specific for metastasis
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- C—CHEMISTRY; METALLURGY
- C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
- C12N—MICROORGANISMS OR ENZYMES; COMPOSITIONS THEREOF; PROPAGATING, PRESERVING, OR MAINTAINING MICROORGANISMS; MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA
- C12N15/00—Mutation or genetic engineering; DNA or RNA concerning genetic engineering, vectors, e.g. plasmids, or their isolation, preparation or purification; Use of hosts therefor
- C12N15/09—Recombinant DNA-technology
- C12N15/63—Introduction of foreign genetic material using vectors; Vectors; Use of hosts therefor; Regulation of expression
- C12N15/79—Vectors or expression systems specially adapted for eukaryotic hosts
- C12N15/85—Vectors or expression systems specially adapted for eukaryotic hosts for animal cells
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- C—CHEMISTRY; METALLURGY
- C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
- C12N—MICROORGANISMS OR ENZYMES; COMPOSITIONS THEREOF; PROPAGATING, PRESERVING, OR MAINTAINING MICROORGANISMS; MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA
- C12N2800/00—Nucleic acids vectors
- C12N2800/10—Plasmid DNA
- C12N2800/106—Plasmid DNA for vertebrates
- C12N2800/107—Plasmid DNA for vertebrates for mammalian
Abstract
The invention provides a novel transcription factor KLF4 capable of regulating and controlling the metastatic capacity of colorectal cancer cells. The transcription factor is combined with a TRIM29 promoter in colorectal cancer cells to regulate the expression level of TRIM29, so that the purpose of regulating the transfer capacity of the colorectal cancer cells is realized. The transcription factor KLF4 realizes the mechanism for regulating the colorectal cancer cell transfer capacity: the transcription factor KLF4 is in positive correlation with the expression of TRIM29, the over-expression of KLF4 can improve the expression of TRIM29, and the high expression of TRIM29 can weaken the transfer capacity of colorectal cancer cells. Therefore, the transcription factor KLF4 is over-expressed to inhibit the metastasis of colorectal cancer cells. Therefore, the transcription factor KLF4 can be used as a drug target for inhibiting colorectal cancer metastasis.
Description
Technical Field
The invention relates to the technical field of bioengineering, and particularly relates to application of a high-efficiency transcription factor KLF4 in regulation and control of colorectal cancer metastasis.
Background
Colorectal cancer (CRC) is a common tumor in the world today. Statistics published by the american cancer society in 2020 suggest that colorectal cancer has risen to the second leading cause of cancer-related death, and the main cause of death in patients is invasion and metastasis of cancer, and the rising death rate year by year makes greater and greater importance to the diagnosis and treatment of colorectal cancer.
In the past decade, the treatment of CRC has made significant progress due to advances in surgery, radiotherapy, chemotherapy, immunotherapy, but tumor metastasis remains one of the most clinically complex and important problems of colorectal cancer. Tumor metastasis is performed in multiple steps, and has multiple involved genes, and the process is complex, for example, tumor is detached from the primary site and fused with surrounding stroma, tumor cells enter the circulatory system and lymphatic system, adhere to endothelial cell walls, gradually extend to blood vessels or a larger area, and the phenomenon of blood vessel proliferation occurs, and finally, a new metastasis is formed. At present, colorectal cancer metastasis is mainly treated after occurrence, and a good means for prediction and prevention is not provided yet, so that colorectal cancer metastasis is killed in an initial stage.
With the continuous development of various medical technologies and the development of chemotherapeutic drugs and targeted drugs, the clinical treatment effect of colorectal cancer patients is greatly improved, but the survival rate of most patients is not improved in terms of long-term survival rate, so that the condition is mainly caused by that micro metastasis of the focus of colorectal cancer patients occurs before radical surgery is performed, and the key point of colorectal cancer prevention and treatment is to control tumor metastasis. At present, the mechanism of colorectal cancer metastasis is less understood clinically, so that the related measures for preventing and treating tumor invasion and metastasis are limited. Colorectal cancer metastasis is an important factor for poor prognosis of colorectal cancer, and no good prevention and treatment means is provided for metastatic colorectal cancer. Therefore, finding and explaining the occurrence of colorectal cancer metastasis is of particular importance.
Disclosure of Invention
In order to solve the technical problems, the invention finds that the expression of the KLF4 gene is obviously different between normal tissues and colorectal cancer tissues by searching a TCGA database, and suggests that the KLF4 gene is possibly used as a marker of colorectal metastasis. The present invention achieves the object of the present invention by the following aspects.
In a first aspect: the invention provides application of a transcription factor KLF4 in preparing a preparation or a medicament for regulating and controlling the expression of TRIM29 in colorectal cancer cells. Through screening of transcription factors influencing the expression of TRIM29 in JASPAR database, the applicant finds that KLF4 has a binding site in the promoter region of TRIM29, and the expression level of the transcription factor KLF4 can influence the expression level of TRIM29 in colorectal cancer cells.
Further, the transcription factor KLF4 regulates expression of TRIM29 by binding to the TRIM29 promoter CCCCCTCCCC region in colorectal cancer cells. The applicant predicts a potential transcription factor binding site in the promoter region of the TRIM29 of colorectal cancer cells through biological information software, and finally shows that the transcription factor KLF4 is bound in the CCCCCTCCCC region of the TRIM29 promoter, so that KLF4 can regulate the expression of TRIM29 by binding to the transcription initiation point of TRIM 29.
In a second aspect: the invention provides application of a transcription factor KLF4 in preparing a medicine for inhibiting colon cancer metastasis. The expression level of the transcription factor KLF4 in the normal tissue and the colorectal cancer tissue is obviously different. The transcription factor KLF4 was expressed at higher levels in normal tissues and at lower levels in colorectal cancer tissues.
Further, the transcription factor KLF4 inhibits metastasis of colorectal cancer cells by increasing the expression level of TRIM29 in the colorectal cancer cells. The applicant discovers that TRIM29 can obviously increase in mRNA level and protein level after KLF4 is overexpressed by transfecting an overexpression vector of a transcription factor KLF4 of colorectal cancer cells in vitro, and regulates the expression up-regulation of TRIM29 to weaken the transfer capacity of the colorectal cancer cells.
Further, the transcription factor KLF4 increases the expression of TRIM29 by binding to the TRIM29 promoter CCCCCTCCCC region in colorectal cancer cells.
In a third aspect: the invention provides a biological product for regulating and controlling the expression of TRIM29 in colorectal cancer cells, and the biological product comprises a transcription factor KLF4 overexpression vector.
Further, the biological product is a reagent, a kit or a chip.
In a fourth aspect: a medicament for treating colon cancer metastasis, which comprises a transcription factor KLF4 overexpression vector.
Compared with the prior art, the invention has the beneficial effects that: the invention discovers a novel transcription factor KLF4 capable of regulating and controlling the transfer capacity of colorectal cancer cells through biological information software analysis. The transcription factor is combined with a TRIM29 promoter in colorectal cancer cells to regulate the expression level of TRIM29, so that the purpose of regulating the transfer capacity of the colorectal cancer cells is realized. The transcription factor KLF4 realizes the mechanism for regulating the colorectal cancer cell transfer capacity: the transcription factor KLF4 is in positive correlation with the expression of TRIM29, the over-expression of KLF4 can improve the expression of TRIM29, and the high expression of TRIM29 can weaken the transfer capacity of colorectal cancer cells. Therefore, the transcription factor KLF4 is over-expressed to inhibit the metastasis of colorectal cancer cells. Therefore, the transcription factor KLF4 can be used as a drug target for inhibiting colorectal cancer metastasis.
Drawings
FIG. 1 is a graph comparing the results of KLF4 expression in normal and colorectal cancer tissues in the TCGA database;
FIG. 2 is a graph of the results of a metastasis experiment overexpressing KLF4 in colorectal cancer cells;
FIG. 3 is a schematic representation of the relationship between the transcription factor KLF4 and TRIM 29; a is a result chart of the fact that the promoter region of TRIM29 in JASPAR has a KLF4 binding site; b is a graph of the effect of TRIM29 on mRNA levels after over-expression of KLF 4; c is a graph of the results of influencing TRIM29 at the protein level after over-expression of KLF 4.
FIG. 4 is a graph showing the results of a metastasis assay in which TRIM29 is overexpressed in colorectal cancer cells.
Detailed Description
In order to show technical solutions, purposes and advantages of the present invention more concisely and clearly, the technical solutions of the present invention are described in detail below with reference to specific embodiments. Unless otherwise specified, the reagents involved in the examples of the present invention are all commercially available products, and all of them are commercially available.
Example 1
The present applicant analyzed the expression level of KLF4 in human normal tissues and colorectal cancer tissues on TCGA, searched KLF4 in TCGA database (https:// portal.gdc.cancer.gov /), analyzed the expression level of KLF4 in colorectal cancer tissues and paired normal tissues, analyzed their differential expression by statistical software, and the results are shown in FIG. 1, showing that KLF4 is under-expressed in colorectal cancer.
Example 2
In an in vitro experiment, for colorectal cancer SW480 cells, a plasmid pcDNA3.1-HA-KLF4 or a control plasmid pcDNA3.1, which is over-expressed by KLF4, is transfected into SW480 by using a plasmid transfection reagent, so that the over-expression plasmid or a blank plasmid of KLF4 is over-expressed, after 12h of transfection, after digestion of the cells, 60000 cells are respectively paved in a chamber of TRANSWELL plates, then 500 mu L of a culture medium containing 10% FBS is added into the plate, TRANSWELL transfer experiments are carried out, and the result is observed after 36 h. The results are shown in fig. 2, which shows that KLF4 over-expressed cells more than the control group in TRANSWELL plates of metastatic cells, suggesting enhanced metastatic capacity, suggesting that the upregulation of KLF4 significantly increased the metastatic capacity of colorectal cancer cells.
Example 3
As a result of finding KLF4 having a binding site in the promoter region of TRIM29 in JASPAR database (http:// JASPAR. genereg. net /), KLF4 was shown in FIG. 3A as a transcription factor of TRIM 29; in vitro experiments, colorectal cancer SW480 cells were transfected with KLF4 overexpression plasmid and control plasmid, and mRNA levels of TRIM29, KLF4 and GAPDH were detected by a fluorescent quantitative PCR (RT-qPCR) detection kit, primers thereof are shown in Table 1, reaction system is shown in Table 2, and reaction procedures: preheating at 94 deg.C for 5 min; entering the circulation of 94 ℃,50s → 50 ℃, 30s → 72 ℃, 30s and circulating 45 times. The gene expression level is relatively quantified by a delta-delta CT analysis method; the Western blotting test kit detects the protein levels of TRIM29, KLF4 and GAPDH, and the sources of the used antibodies are shown in Table 3; the expression level of TRIM29 was found to increase significantly at the mRNA and protein levels after overexpression of KLF4, and the results are shown in fig. 3B, 3C, suggesting that KLF4 may regulate the up-regulation of TRIM29 by binding to the transcription initiation point of TRIM 29.
TABLE 1 RT-qPCR primers
TABLE 2 RT-qPCR reaction System
TABLE 3 antibody origin information
Example 4
In vitro experiments, colorectal cancer SW480 cells are transfected with TRIM29 overexpression plasmids and control plasmids, and then are respectively plated to carry out TRANSWELL transfer experiments, so that the fact that the cells over-expressed by TRIM29 are more than the transfer cells of a control group in a TRANSWELL plate is shown, the transfer capacity is enhanced, the fact that the cell transfer capacity of colorectal cancer is obviously improved due to the up-regulation of TRIM29 is shown, and the experiment results of the above examples are combined, and the fact that the cell transfer capacity of colorectal cancer can be further promoted by efficiently up-regulating TRIM29 after KLF4 is up-regulated is shown in fig. 4.
Finally, it should be noted that the above embodiments are only used for illustrating the technical solutions of the present invention and not for limiting the protection scope of the present invention, and although the present invention is described in detail with reference to the preferred embodiments, it should be understood by those skilled in the art that modifications or equivalent substitutions can be made on the technical solutions of the present invention without departing from the spirit and scope of the technical solutions of the present invention.
Claims (8)
1. Application of transcription factor KLF4 in preparing a preparation or a medicament for regulating the expression of TRIM29 in colorectal cancer cells.
2. The use of claim 1, wherein the transcription factor KLF4 regulates the expression of TRIM29 by binding to the region of TRIM29 promoter CCCCCTCCCC in colorectal cancer cells.
3. Application of transcription factor KLF4 in preparing medicine for inhibiting colon cancer metastasis is provided.
4. The use of claim 3, wherein the transcription factor KLF4 inhibits metastasis of colorectal cancer cells by increasing the expression level of TRIM29 in colorectal cancer cells.
5. The use of claim 4, wherein the transcription factor KLF4 increases the expression of TRIM29 by binding to the CCCCCTCCCC region of the TRIM29 promoter in colorectal cancer cells.
6. A biological product for regulating the expression of TRIM29 in colorectal cancer cells, wherein the biological product comprises a transcription factor KLF4 overexpression vector.
7. The biological product according to claim 6, wherein the biological product is a reagent, a kit or a chip.
8. A medicament for treating colon cancer metastasis, which comprises a transcription factor KLF4 overexpression vector.
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Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN103320500A (en) * | 2013-05-30 | 2013-09-25 | 上海交通大学医学院附属新华医院 | Method for promoting colorectal cancer (CRC) distant metastasis by microRNA-29a through KLF4 |
| US20150099775A1 (en) * | 2013-10-04 | 2015-04-09 | Aptose Biosciences Inc. | Compositions and methods for treating cancers |
| US20150366835A1 (en) * | 2014-06-12 | 2015-12-24 | Nsabp Foundation, Inc. | Methods of Subtyping CRC and their Association with Treatment of Colon Cancer Patients with Oxaliplatin |
-
2021
- 2021-04-06 CN CN202110366085.5A patent/CN113134077A/en active Pending
Patent Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN103320500A (en) * | 2013-05-30 | 2013-09-25 | 上海交通大学医学院附属新华医院 | Method for promoting colorectal cancer (CRC) distant metastasis by microRNA-29a through KLF4 |
| US20150099775A1 (en) * | 2013-10-04 | 2015-04-09 | Aptose Biosciences Inc. | Compositions and methods for treating cancers |
| US20150366835A1 (en) * | 2014-06-12 | 2015-12-24 | Nsabp Foundation, Inc. | Methods of Subtyping CRC and their Association with Treatment of Colon Cancer Patients with Oxaliplatin |
Non-Patent Citations (7)
| Title |
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| JING HAN等: "Transcriptional dysregulation of TRIM29 promotes colorectal cancer carcinogenesis via pyruvate kinase-mediated glucose metabolism" * |
| JUNTAO SUN等: "TRIM29 facilitates the epithelial-to-mesenchymal transition and the progression of colorectal cancer via the activation of the Wnt/β-catenin signaling pathway", 《JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH》 * |
| YONGZHENG MA等: "KLF4 inhibits colorectal cancer cell proliferation dependent on NDRG2 signaling", 《ONCOL REP》 * |
| 宋刚等: "MicroRNA-10b在大肠癌中的表达及其对SW480细胞侵袭转移的影响", 《解剖科学进展》 * |
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