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The Relationship Between CTNNB1 Gene Mutation and the Classic Wnt/β-Catenin Signaling Pathway

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With the development of science and technology, tumor research has gone from routine pathological examinations to molecular and gene levels. The study of the pathogenesis of cancer molecular biology is of great significance for early cancer diagnosis and cancer treatment methods. In recent years, molecular biology technology has been widely used in experiments, and more and more companies have provided molecular biology services. CTNNB1 is a proto-oncogene that encodes β-Catenin protein, and β-catenin can bind to APC protein, and mutations can lead to colorectal cancer, piloblastoma, medulloblastoma and ovarian cancer.

CTNNB1 gene

CTNNB1 gene is located on chromosome 3p21, and β-catenin is the protein that it encodes. CTNNB1 is closely related to the occurrence and development of tumors. Increased expression of this protein can be seen in tumor tissues such as liver cancer, colon cancer, gastric cancer and lung cancer. For example, to explore the effect of CTNNB1 silencing on the proliferation of ovarian cancer cells, human ovarian cancer SKOV3 cells were cultured in vitro and randomly divided into blank control group, negative control group and CTN experimental group, and then transfected into the shRNA vector plasmid targeting CTNNB1. The protein expression of CTNNB1 and cell viability were detected by western blot analysis and MMT. The study found that down-regulation of CTNNB1 gene expression can inhibit the proliferation of ovarian cancer SKOV3 cells.

Abnormal Wnt signal transduction is considered to be the key to the process of ovarian cancer. In the process of activating the Wnt pathway, the stability of CTNNB1 protein is crucial, providing a powerful target for new treatments of ovarian cancer. At present, tumor research has penetrated into the molecular level, oncogenes, tumor suppressor genes, and the instability of microsatellites. Commonly used molecular biology detection techniques include gene sequence analysis, polymerase chain reaction, fluorescence in situ hybridization, , Gene chip technology and high-throughput sequencing technology. Molecular biology technology is an important means of medicine and life science research and practice at this stage. Medicilon can provide customers with molecular biology services to support the screening and development of macromolecular drugs, small molecule drugs, biologics, vaccines and biomarkers, as well as their preclinical and clinical research.

It is of great significance to strengthen the research on the molecular biology of craniopharyngiomas. More in-depth basic research on the molecular biology of craniopharyngiomas will help to find effective molecular targets for targeted therapy. The diagnosis, prognostic evaluation and treatment of the disease open up new ways and ideas. For example, in the study on the molecular biological mechanism of enamel-type craniopharyngioma (ACP), it was found that the mutation of CTNNB1 gene caused the Wnt pathway to be abnormally activated, and Wnt ligand competitively binds to the receptor on the membrane to inhibit GSK-39 It binds to receptors on the membrane, thereby preventing the formation of β-Catenin degradation complex, allowing β-Catenin to accumulate in the cytoplasm, and finally translocate into the nucleus, thereby promoting the transcription of β-Catenin target genes and stimulating cell proliferation and other The process of Wnt regulation [1].

The Wnt/β-Catenin activation pathway has been confirmed in a variety of human tumors, and studies have also found that the activation of Wnt/β-Catenin target genes can cause tumor cell invasion, metastasis and proliferation. Cell experiments also found that ACP cells with high expression of β-Catenin and activation of target genes have increased migration and invasiveness. The accumulation of β-Catenin can occur in the cell clusters of tumor invasive protrusions and can enter normal brain tissue. The study also found that mutations in the exon 3 of CTNNB1 gene caused β-Catenin nuclear accumulation. Therefore, nuclear accumulation of β-Catenin becomes the histological hallmark of CTNNB1 mutation. According to literature reports, about 69%-100% of CTNNBl mutations exist in ACP.

The activation of β-Catenin aggregated cell clusters caused by CTNNB1 mutation may be related to the occurrence of some cancers. Through the study of molecular biological mechanisms of cancer, it can provide an important research basis for the research of tumor treatment methods, so strengthen the tumor molecular biology The study of science is of great significance.

[1] Research progress in molecular biology mechanism of craniopharyngioma[J].

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