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    Home > Active Ingredient News > Antitumor Therapy > Br J Cancer: EEF1A2 mediates the epitheline-interstital transformation process to promote the metastasis of pulmonary adenocarcinoma

    Br J Cancer: EEF1A2 mediates the epitheline-interstital transformation process to promote the metastasis of pulmonary adenocarcinoma

    • Last Update: 2021-02-01
    • Source: Internet
    • Author: User
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    Lung cancer is one of the most common malignancies, with 1.77 million lung cancer deaths worldwide each year.
    lung cancer are divided into two main categories, non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC).
    includes lung adenocarcinoma (LUAD) and squamous cell carcinoma (SCC), accounting for about 80-85% of all lung cancer cases.
    Although previous studies have revealed the expression characteristics of targeted KRAS and EGFR mutations and EML4-ALK fusion genes in LUAD and developed appropriate treatment strategies, the total five-year survival rate for lung adenocarcinoma patients is still very low, at only 18%.
    5-year survival rate, especially in patients with advanced lung adenocarcinoma, was only 2-8%.
    , there is an urgent need to better understand the potential key transfer mechanisms for LUAD development.
    EEF1A2 (the epinephrine translation extension factor 1 alpha2) is a cancer-causing gene that promotes the development of breast and pancreatic cancer.
    study aims to shed light on the carcinogenic effects of EEF1A2 in the metastasis of lung adenocarcinoma (LUAD).
    The expression level and clinical significance of EEF1A2 in pulmonary adenocarcinoma researchers studied the expression level of EEF1A2 in LUAD tissues and cells through immunological and protein brination experiments, and further studied the role of EEF1A2 in the development of LUAD.
    LC-MS mass spectromety identified potential EEF1A2 binding proteins and determined protein interactions through immunofluorescence and immunosuppression (Co-IP) experiments.
    researchers have found that EEF1A2 mediates the endocal-interstational transformation (EMT) process and facilitates the transfer of LUAD cells.
    addition, EEF1A2 is able to interact with HSP90AB1, increase the expression of T-beta RI and T-beta RII, and improve the expression level and nucleation of SMAD3 and pSMAD3, ultimately promoting the EMT process of LUAD cells.
    further studies have shown that the over-expression levels of EEF1A2 in tumor tissue correspond to poor prognostic differences and shorter lifetimes in LUAD patients.
    silent EEF1A2 inhibits tumor growth and metastasis in general, the results reveal the molecular function of EEF1A2 in LUAD metastasis, EEF1A2 may be a potential target for LUAD.
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