Dataset Information

IMPDH2 promotes cell proliferation and epithelial-mesenchymal transition of non-small cell lung cancer by activating the Wnt/?-catenin signaling pathway.

ABSTRACT: 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/?-catenin signaling pathway by decreasing the expression levels of Wnt3a and ?-catenin, while increasing the expression levels of phosphorylated glycogen synthase kinase-3? in NSCLC cells. These findings of the present study indicated that IMPDH2 may promote NSCLC progression by activating the Wnt/?-catenin signaling pathway, which suggested that IMPDH2 may be a novel therapeutic target for patients with NSCLC.

SUBMITTER: Xu H

PROVIDER: S-EPMC7491058 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

IMPDH2 promotes cell proliferation and epithelial-mesenchymal transition of non-small cell lung cancer by activating the Wnt/β-catenin signaling pathway.

Xu Hao H Ma Hongda H Zha Lifen L Li Qian Q Yang Guanghui G Pan Huiming H Fei Xiangping X Xu Xingxiang X Xing Chen C Zhang Ladi L

Oncology letters 20200909 5

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 ...[more]

PMID: 32963625

Similar Datasets

Project description:Osteosarcoma (OS) is a rare type of tumor and mostly occurs in children and adolescents. Approximately 10‑25% of patients with OS have lung metastases, and lung damage caused by lung metastasis is the main cause of mortality. Therefore, studying the growth and metastasis of OS is key in reducing OS mortality and improving prognosis. The expression of long non‑coding RNA (lncRNA) cancer susceptibility 15 (CASC15) in OS patients or OS cell lines were quantified by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). The expression of vimentin, E‑cadherin, N‑cadherin, and cyclin D were detected by RT‑qPCR and western blotting. Mice were injected with OS cell lines via the tail vein to observe tumor formation in the lung. CCK‑8 and EdU assays were utilized to evaluate cell proliferation. Both Ttranswell assay and cell scratch test detected cell migration. The results revealed that lncRNA‑CASC15 was highly expressed in clinical samples and OS cells. In vitro verification experiments revealed that CASC15 promoted the growth of OS cells. Rescue experiments demonstrated that CASC15 affected the cell cycle by activating the Wnt/β‑catenin pathway, thereby promoting cell proliferation. Furthermore, the transfection dose test indicated that lentiviruses expressing various doses of CASC15‑overexpression (oe‑CASC15) altered the proliferation and migration status of OS cells. CASC15 promoted OS cell metastasis both in vivo and in vitro. The overexpression of CASC15 revealed that the occurrence of metastasis was also related to the Wnt/β‑catenin pathway. The western blotting results revealed that CASC15 could lead to β‑catenin entering the nucleus via the Wnt pathway to promote the epithelial‑mesenchymal transition (EMT) of OS cells. To sum up, CASC15 promoted the proliferation of OS cells in vitro and the growth of OS xenograft tumors in vivo. Moreover, CASC15 promoted the entry of β‑catenin into the nucleus, thus activating the Wnt pathway and subsequently promoting the EMT of OS cells.

Dataset Information

IMPDH2 promotes cell proliferation and epithelial-mesenchymal transition of non-small cell lung cancer by activating the Wnt/?-catenin signaling pathway.

Publications

IMPDH2 promotes cell proliferation and epithelial-mesenchymal transition of non-small cell lung cancer by activating the Wnt/β-catenin signaling pathway.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets