IMPDH2 promotes cell proliferation and epithelial-mesenchymal transition of non-small cell lung cancer by activating the Wnt/β-catenin signaling pathway
Autor: | Xingxiang Xu, Hao Xu, Ladi Zhang, Chen Xing, Xiangping Fei, Lifen Zha, Guanghui Yang, Huiming Pan, Qian Li, Hongda Ma |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Cancer Research Oncogene Cell growth Chemistry Cell Wnt signaling pathway Articles Cell cycle Molecular medicine respiratory tract diseases 03 medical and health sciences 030104 developmental biology 0302 clinical medicine medicine.anatomical_structure Oncology 030220 oncology & carcinogenesis medicine Cancer research Epithelial–mesenchymal transition Signal transduction |
Zdroj: | Oncol Lett |
ISSN: | 1792-1074 |
Popis: | Inosine 5'-monophosphate dehydrogenase type II (IMPDH2) is an important enzyme involved in the biosynthesis of guanine nucleotides. Therefore, the present study aimed to investigate the potential and molecular mechanism of IMPDH2 in non-small cell lung cancer (NSCLC). Reverse transcription-quantitative PCR and immunohistochemistry were used to detect IMPDH2 expression levels in NSCLC tissues and cells. A Cell Counting Kit-8 assay, colony formation assay, flow cytometry, wound healing, Transwell assay, western blotting and immunofluorescence analyses were utilized to identify the effects of upregulated IMPDH2 levels on NSCLC cells. The expression levels of IMPDH2 have been discovered to be upregulated in several types of human cancer; however, the biological and clinical value of IMPDH2 in NSCLC remains unclear. The results of the present study revealed that the expression levels of IMPDH2 were significantly upregulated in NSCLC tissues. Furthermore, the genetic knockdown of IMPDH2 significantly hindered the proliferation, apoptosis, invasion, migration and epithelial-mesenchymal transition of NSCLC cells, whereas the overexpression of IMPDH2 achieved the opposite results. In addition, the results of the present study demonstrated that the inhibition of IMPDH2 inhibited the Wnt/β-catenin signaling pathway by decreasing the expression levels of Wnt3a and β-catenin, while increasing the expression levels of phosphorylated glycogen synthase kinase-3β in NSCLC cells. These findings of the present study indicated that IMPDH2 may promote NSCLC progression by activating the Wnt/β-catenin signaling pathway, which suggested that IMPDH2 may be a novel therapeutic target for patients with NSCLC. |
Databáze: | OpenAIRE |
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