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CN-122013327-A - ShRNA interference library and vector for inhibiting CT45A3 expression and application of shRNA interference library and vector in anti-colon cancer drugs

CN122013327ACN 122013327 ACN122013327 ACN 122013327ACN-122013327-A

Abstract

The invention discloses an shRNA interference library and a vector for inhibiting CT45A3 expression and application of the shRNA interference library and the vector in anti-colon cancer drugs, and belongs to the technical field of gene drugs. The shRNA interference library comprises one or more of sequences shown in SEQ ID NO. 1-3. The shRNA interference library or the expression vector thereof can efficiently and specifically down regulate the expression level of CT45A3 in colorectal cancer cells, thereby blocking the abnormal activation of downstream cancer promotion signal channels mediated by the shRNA interference library and obviously inhibiting the progress of malignant phenotype. The shRNA interference library has potential clinical application value in targeted treatment of colorectal cancer.

Inventors

  • WAN CHUNHUA
  • HU BAOYING
  • ZHAO JIANYA
  • LI TIANHAO

Assignees

  • 南通大学

Dates

Publication Date
20260512
Application Date
20260226

Claims (9)

  1. 1. The shRNA interference library for inhibiting CT45A3 expression is characterized by comprising one or more of sequences shown in SEQ ID NO.1, SEQ ID NO.2 and SEQ ID NO. 3.
  2. 2. The shRNA interference library of claim 1, wherein the shRNA interference library comprises the sequences set forth in SEQ ID No.1, SEQ ID No.2, and SEQ ID No. 3.
  3. 3. The shRNA interference library of claim 2, wherein the molar ratio of sequences shown in SEQ ID No.1, SEQ ID No.2 and SEQ ID No.3 in the shRNA interference library is 1:1:1.
  4. 4. An expression vector comprising the shRNA interference library of any one of claims 1-3.
  5. 5. Use of the shRNA interference library of any one of claims 1-3 or the expression vector of claim 4 in the preparation of a medicament for inhibiting expression of CT45 A3.
  6. 6. The use according to claim 5, wherein the medicament is a medicament for inhibiting expression of CT45A3 in colon cancer cells.
  7. 7. Use of the shRNA interfering library of any one of claims 1-3 or the expression vector of claim 4 in the preparation of an anti-colon cancer medicament.
  8. 8. The use according to claim 7, wherein the antitumor agent is for inhibiting expression of oncogenes MYC and Cyclin D1 in colon cancer cells.
  9. 9. The use according to claim 7, wherein the antineoplastic agent is for inhibiting the proliferative capacity of colon cancer cells.

Description

ShRNA interference library and vector for inhibiting CT45A3 expression and application of shRNA interference library and vector in anti-colon cancer drugs Technical Field The invention belongs to the technical field of gene medicines, and particularly relates to an shRNA interference library and a vector for inhibiting CT45A3 expression and application of the shRNA interference library and the vector in anti-colon cancer medicines. Background Colorectal cancer is a complex process involving multiple factors and steps, and is commonly influenced by genetic background, environmental factors, life style and other aspects. Family genetic history, particularly hereditary colorectal cancer syndrome, is one of its important risk factors. In addition, obesity, long-term high fat Gao Reliang diet, excessive intake of red meat and processed meat products, type 2 diabetes, insulin resistance, chronic inflammatory bowel disease (such as ulcerative colitis and Crohn's disease), insufficient intake of dietary fiber, smoking, excessive drinking, and the like have also been shown to be closely related to the occurrence of colorectal cancer. Currently, for patients with early colorectal cancer, clinical surgery is the primary choice, often in combination with preoperative or postoperative adjuvant chemotherapy, a better prognosis is usually obtained. However, for patients with metastatic colorectal cancer, the treatment strategies mainly include chemotherapy, targeted therapy and immunotherapy, as the best surgical occasion has been missed. However, even with these systemic treatment regimens, patients are still at extremely high risk of relapse, with generally poor overall prognosis. The bottleneck of the clinical treatment enables the development of novel therapeutic targets from the molecular level to be a research focus for breaking through the current dilemma. Colorectal cancer often occurs with disturbances in epigenetic regulation, particularly alterations in the methylation state of genes, which in turn lead to abnormal activation of genes that are not expressed in part in normal somatic cells. Cancer/testis antigens (Cancer/TESTIS ANTIGEN, CT antigens) are a class of proteins that are expressed only in testis in normal tissues, but are aberrantly expressed in a variety of tumors. The coding genes are usually in a highly methylated state in normal somatic cells, transcription is strictly inhibited, and in tumors such as colorectal cancer, the genes are re-expressed due to abnormal methylation and participate in malignant transformation and proliferation processes of the tumors. Therefore, CT antigen has important clinical application potential and can be used as a diagnostic marker and a candidate molecule for targeted treatment. At present, more than hundred CT antigen genes have been identified in human genome, but the research on specific functions and regulation mechanisms thereof in tumors is still relatively limited, and CT antigens capable of serving as effective intervention targets are deficient. Therefore, the development of novel CT antigen targets with key driving roles in colorectal cancer and the development of corresponding efficient, specific intervention strategies has become an urgent need to drive the optimization of colorectal cancer clinical therapies. Disclosure of Invention Aiming at the problems in the prior art, the invention aims to provide an shRNA interference library and a vector for inhibiting CT45A3 expression and application thereof in anti-colon cancer drugs. In a first aspect of the invention, there is provided a shRNA interference library for inhibiting CT45A3 expression, the shRNA interference library comprising one or more of the sequences shown in SEQ ID NO.1, SEQ ID NO.2 and SEQ ID NO. 3. In some embodiments, the shRNA interference library comprises the sequences set forth in SEQ ID No.1, SEQ ID No.2, and SEQ ID No. 3. In some embodiments, the molar ratio of the sequences set forth in SEQ ID NO.1, SEQ ID NO.2, and SEQ ID NO.3 in the shRNA interference library is 1:1:1. In some embodiments, the expression vector contains a library of shRNA interference as described above. In a second aspect, the invention provides an application of the shRNA interference library or the expression vector in preparation of a medicament for inhibiting CT45A3 expression. In some embodiments, the agent is an agent that inhibits CT45A3 expression in colon cancer cells. In a third aspect, the invention provides an application of the shRNA interference library or the expression vector in preparation of anti-colon cancer drugs. In some embodiments, the anti-tumor agent is used to inhibit expression of oncogenes MYC and Cyclin D1 in colon cancer cells. In some embodiments, the anti-tumor agent is used to inhibit the proliferative capacity of colon cancer cells. Compared with the prior art, the invention constructs a plurality of DNA sequences corresponding to the shRNA of CT45A3 to the pLKO.1 eukaryotic e