Dataset Information

DHX9 inhibits epithelial-mesenchymal transition in human lung adenocarcinoma cells by regulating STAT3.

ABSTRACT: DHX9 has numerous functions regulating transcription, translation, RNA processing and transport, and DNA replication and maintenance of genomic stability. It is involved in human cancers as either an oncogene or tumor suppressor. However, its role in the progression of lung cancer and underlying mechanisms remains unclear. In this study, we demonstrated that DHX9 is overexpressed in human lung cancer tissues and serum. Also, a favorable prognosis of lung adenocarcinoma is predicted when DHX9 is at a high level. DHX9 knockdown promoted cell proliferation, migration, and invasion and inhibited apoptosis progression in A549 cells. Moreover, DHX9 knockdown led to a significant decrease of E-cadherin expression, an increase of vimentin and snail, and a significant increase in the phosphorylation of STAT3 in A549 cells. In summary, our studies identified a novel role of DHX9 in driving tumor growth and epithelial-mesenchymal transition progress of A549 cells. We propose that the STAT3 pathway may be implicated in the DHX9-related epithelial-mesenchymal transition of lung adenocarcinoma. Therefore, DHX9 may be a prognostic marker or potential therapeutic target for lung adenocarcinoma.

SUBMITTER: Yan X

PROVIDER: S-EPMC6731401 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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DHX9 inhibits epithelial-mesenchymal transition in human lung adenocarcinoma cells by regulating STAT3.

Yan Xueli X Chang Jing J Sun Ruiying R Meng Xia X Wang Wei W Zeng Lizhong L Liu Boxuan B Li Wei W Yan Xuehua X Huang Chen C Zhao Yongxi Y Li Zongfang Z Yang Shuanying S

American journal of translational research 20190815 8

DHX9 has numerous functions regulating transcription, translation, RNA processing and transport, and DNA replication and maintenance of genomic stability. It is involved in human cancers as either an oncogene or tumor suppressor. However, its role in the progression of lung cancer and underlying mechanisms remains unclear. In this study, we demonstrated that DHX9 is overexpressed in human lung cancer tissues and serum. Also, a favorable prognosis of lung adenocarcinoma is predicted when DHX9 is ...[more]

PMID: 31497206

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Project description:BackgroundLung cancer is the most common and lethal malignancy worldwide. TCTP is highly expressed in various cancers including lung cancer. Epithelial-mesenchymal transition (EMT) could increase cancer cell invasion. Whether TCTP's expression is associated with EMT in lung adenocarcinoma is largely unknown.MethodsSeveral Gene Expression Omnibus datasets were used to analyze the correlation between TCTP expression and overall survival of lung adenocarcinoma patients by Kaplan-Meier survival analysis. Then, 24 surgically removed fresh lung adenocarcinoma tissue samples and paired paracancer tissue samples were used to analyze the correlation between TCTP expression and tumor stage by immunohistochemical analysis. Furthermore, stable cell lines were generated using lentiviral transduction systems to knock down or overexpress TCTP in A549 cells. Cell migration and invasion were measured by scratch and transwell assays, and EMT marker proteins such as α-SMA, ZEB1, and E-cadherin were quantitated by Western blot. The expression levels of miR-200a, miR-141, and miR-429 were determined by real-time quantitative PCR, and their target genes were predicted by an online database miRTarBase. The interaction between TCTP and these genes was analyzed by String database and visualized by Cytoscape.ResultsTCTP was highly expressed in tumor tissues compared to paracancer tissues. The expression of TCTP was associated with shorter overall survival. TCTP knockdown experiment in A549 cells suggested that TCTP knockdown could decrease the migration and invasion of lung cancer cells, and the expression level of ZEB1 and α-SMA, but increase the expression of E-cadherin and p53. Vice versa, overexpression of TCTP could increase the migration and invasion of cancer cells, and the expression level of ZEB1 and α-SMA, but decrease the expression of E-cadherin and p53. Furthermore, we found the expression of miR-200a, miR-141, and miR-429 was associated with TCTP expression.ConclusionTCTP promotes EMT in lung adenocarcinoma, and this effect may be associated with miR-200 family members like miR-200a, miR-141, and miR-429.

Dataset Information

DHX9 inhibits epithelial-mesenchymal transition in human lung adenocarcinoma cells by regulating STAT3.

Publications

DHX9 inhibits epithelial-mesenchymal transition in human lung adenocarcinoma cells by regulating STAT3.

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