NDLI: Transcription factor glioma-associated oncogene homolog 1 is required for transforming growth factor-ß1-induced epithelial-mesenchymal transition of non-small cell lung cancer cells.

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Transcription factor glioma-associated oncogene homolog 1 is required for transforming growth factor-ß1-induced epithelial-mesenchymal transition of non-small cell lung cancer cells.

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Transcription factor glioma-associated oncogene homolog 1 is required for transforming growth factor-ß1-induced epithelial-mesenchymal transition of non-small cell lung cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Li, Hua Long, Xiao-Hong Zhang, Xian-Quan Da, Li-Jun Fan, Wei-Dong
Description	Author Affiliation: Li H ( Department of Oncology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.); Da LJ ( Department of Oncology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.); Fan WD ( Department of Oncology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.); Long XH ( Department of Oncology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.); Zhang XQ ( Department of Oncology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.)
Abstract	Epithelialmesenchymal transition (EMT) is the process by which epithelial cells depolarize and acquire a mesenchymal phenotype, and is a common early step in the process of metastasis. Patients with lung cancer frequently already have distant metastases when they are diagnosed, highlighting the requirement for early and effective interventions to control metastatic disease. Transforming growth factorß1 (TGFß1) is able to induce EMT, however the molecular mechanism of this remains unclear. In the current study, TGFß1 was reported to induce EMT and promote the migration of nonsmall cell lung cancer (NSCLC) cells. A notable observation was that EMT induction was accompanied by the upregulation of human gliomaassociated oncogene homolog 1 (Gli1) mRNA and protein levels. Furthermore, Gli1 levels were depleted by small interfering RNA, and the Gli1 inhibitor GANT 61 attenuated the TGFß1mediated induction of EMT and cell migration. The results of the current study suggest that Gli1 regulates TGFß1induced EMT, which may provide a novel therapeutic target to inhibit metastasis in patients with NSCLC.
ISSN	17912997
e-ISSN	17913004
DOI	10.3892/mmr.2015.3150
Journal	Molecular Medicine Reports
Issue Number	5
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Carcinoma, Non-small-cell Lung Genetics Pathology Epithelial-mesenchymal Transition Drug Effects Lung Neoplasms Transcription Factors Transforming Growth Factor Beta1 Pharmacology Cell Line, Tumor Cell Movement Gene Expression Regulation, Neoplastic Rna Interference Rna, Small Interfering Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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