GTPBP4: A New Therapeutic Target Gene Promotes Tumor Progression in Non-Small Cell Lung Cancer via EMT.
GTPBP4: A New Therapeutic Target Gene Promotes Tumor Progression in Non-Small Cell Lung Cancer via EMT.
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GTPBP4:一种新的治疗靶基因通过 EMT 促进非小细胞肺癌的肿瘤进展
DOI:
10.1155/2022/2164897
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发表时间:
2022
影响因子:
--
通讯作者:
Wang, Lixin
中科院分区:
文献类型:
--
作者:
Wu, Junlu;Chen, Guofei;Wang, Weiwei;Yang, Yang;Yuan, Yi;Shang, Anquan;Quan, Wenqiang;Wang, Lixin
Lung cancer has a complex etiology involving multiple regulatory systems. Uncertainty about the biology and evolution of lung cancer has made it difficult to improve its poor prognosis. To create efficient therapeutic targets and optimal molecular screening tools for lung cancer, the most important task seems to be to understand how it develops and progresses. The expression and regulation of GTPBP4 in non-small cell lung cancer (NSCLC) are not well understood. Using methods such as knocking down GTPBP4 in lung cancer cells and establishing a mouse lung cancer model, we found that the expression of GTPBP4 was upregulated in human lung adenocarcinoma cells and tissues, and that knocking down the expression of the GTPBP4 gene in A549 and Calu-1 lung adenocarcinoma cells can inhibit the proliferation of lung adenocarcinoma cells and reduce their invasion ability. The results of the mouse lung cancer model showed that the lung weight and the number of lung surface nodules decreased significantly in the LLC-GTPBP4 KO group. The mechanism by which GTPBP4 regulation affects the progression of lung adenocarcinoma may be related to the regulation of EMT. From this study, new research ideas emerge to explore GTPBP4 as a biomarker and therapeutic target for early diagnosis and treatment of lung cancer.
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影响因子:
--
作者:
Chen J;Zhang J;Zhang Z
通讯作者:
Zhang Z
影响因子:
3.8
作者:
Curtin, GM;Higuchi, MA;Mosberg, AT
通讯作者:
Mosberg, AT
影响因子:
5.7
作者:
Bade, Brett C.;Dela Cruz, Charles S.
通讯作者:
Dela Cruz, Charles S.
影响因子:
5.2
作者:
Landeros N;Santoro PM;Carrasco-Avino G;Corvalan AH
通讯作者:
Corvalan AH
影响因子:
--
作者:
Liu WB;Jia WD;Ma JL;Xu GL;Zhou HC;Peng Y;Wang W
通讯作者:
Wang W