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    Home > Active Ingredient News > Antitumor Therapy > Br J Cancer: The new CD63-BCAR4 fusion protein promotes tumor-causing and metastasis of lung adenocarcinoma

    Br J Cancer: The new CD63-BCAR4 fusion protein promotes tumor-causing and metastasis of lung adenocarcinoma

    • Last Update: 2020-11-25
    • Source: Internet
    • Author: User
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    Patients with pulmonary adenocarcinoma can be classified according to molecular changes that encode genes related to kinases such as EGFR, KRAS, ALK, ROS1, and BRAF.
    the presence of these changes can provide effective targeted treatment for subsethic patients.
    addition, the fusion of cancer-causing genes is an important genetic change driving the development of lung cancer.
    previous studies have shown that the fusion genes of EML4 and ALC have been found in non-small cell lung cancer (NSCLC), followed by stained weight rows of ALC, RET and ROS1, which are considered to be the driving genes of important cancer-causing genes.
    and the relapsed fusion proteins currently identified as being associated with lung cancer have one common feature: all fusion proteins are active kinases with a complete kinase domain.
    , genome-wide studies have shown that fusion variants of the BCAR4 (Breast Cancer Anti-Estrogen Resistance 4) gene have been repeatedly found in lung adenocarcinoma.
    , however, the functional study of the BCAR4 fusion gene has yet to be carried out.
    based on RNA sequencing data analysis, the researchers identified a fusion transcript of CD63-BCAR4 in a Korean lung adenocarcinoma patient who did not carry a known activation mutation of the EGFR and KRAS genes, and studied the carcinogenic effects of CD63-BCAR4 in further experiments.
    tumor-like results of CD63-BCAR4 fusion proteins show that the expression of CD63-BCAR4 fusion proteins in the upper and second sources of bronchopal endocrine can significantly enhance cell migration and cell proliferation.
    the expression of the low BCAR4 fusion gene through small interfering RNA, cell migration was significantly reduced.
    mouse transplant tumor model confirmed the tumor and metastasis ability of CD63-BCAR4 fusion protein.
    by conducting off-the-cortic injections in mice, cells that express fusion proteins can metastransid from their origin to the liver and lungs.
    further studies have shown that Cyclin D1, MMP1, Slug, and interstate markers all show significant increases in the expression of CD63-BCAR4.
    , the results suggest that the newly discovered fusion gene CD63-BCAR4 may be a potential new cancer-causing gene for lung adenocarcinoma.
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