LMO3 promotes gastric cancer cell invasion and proliferation through Akt-mTOR and Akt-GSK3β signaling
Autor: | Hong-Yan Gong, Guang-Jun Liao, Ning-Ning Jiang, Kuai-Yun Yu, Yan Zhou, Yan-Song Qiu |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
proliferation 03 medical and health sciences 0302 clinical medicine GSK-3 Stomach Neoplasms Cell Line Tumor Genetics Humans LIM domain only 3 Neoplasm Invasiveness Protein kinase B GSK3B PI3K/AKT/mTOR pathway mammalian target of rapamycin Adaptor Proteins Signal Transducing Cell Proliferation Glycogen Synthase Kinase 3 beta Chemistry Cell growth gastric cancer Akt TOR Serine-Threonine Kinases General Medicine Articles Cell cycle LIM Domain Proteins invasion Prognosis Gene Expression Regulation Neoplastic 030104 developmental biology glycogen synthase kinase 3β 030220 oncology & carcinogenesis Cancer research Phosphorylation Signal transduction Proto-Oncogene Proteins c-akt Signal Transduction |
Zdroj: | International Journal of Molecular Medicine |
ISSN: | 1791-244X 1107-3756 |
Popis: | The present study assessed the biological functions of LIM domain only 3 (LMO3) in gastric cancer (GC) investigated and the underlying molecular mechanisms. It was revealed that the expression of LMO3 was significantly upregulated in GC tissues. A GC tissue microarray (n=164) indicated that LMO3 expression was closely associated with clinicopathological factors, as well as overall survival and disease-free survival of patients. After knockdown of LMO3 in MGC-803 and SGC-7901 cells, the invasion and proliferation were obviously suppressed. Furthermore, LMO3 knockdown suppressed the phosphorylation of Akt, mammalian target of rapamycin (mTOR) and glycogen synthase kinase (GSK)3β signaling. An inhibitor of mTOR, dactolisib, abrogated recombinant LMO3 protein-induced GC cell invasion and proliferation, while an inhibitor of GSK3β, CHIR-98014, only abrogated rLMO3 protein-induced proliferation. These results suggested that LMO3 promotes GC cell invasion and proliferation mainly through Akt/mTOR and Akt/GSK3β signaling. LMO3 may serve as a potential therapeutic target for GC in the future. |
Databáze: | OpenAIRE |
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