| Title | miR-29b suppresses proliferation, migration, and invasion of tongue squamous cell carcinoma through PTEN-AKT signaling pathway by targeting Sp1 |
| Authors | Jia, Ling-Fei Huang, Yi-Ping Zheng, Yun-Fei Lyu, Ming-Yue Wei, Su-Bi Meng, Zhen Gan, Ye-Hua |
| Affiliation | Peking Univ, Sch & Hosp Stomatol, Dept Oral & Maxillofacial Surg, Beijing 100081, Peoples R China. Peking Univ, Sch & Hosp Stomatol, Mol Biol Lab, Beijing 100081, Peoples R China. Peking Univ, Sch & Hosp Stomatol, Dept Orthodont, Beijing 100081, Peoples R China. Tsinghua Univ, Med Syst Biol Res Ctr, Beijing 100084, Peoples R China. Peking Univ, Sch & Hosp Stomatol, Mol Biol Lab, 22 Zhongguancun Ave South, Beijing 100081, Peoples R China. |
| Keywords | Oral cancer Tongue squamous cell carcinoma miR-29b Sp1 PTEN AKT TRANSCRIPTION FACTOR SP1 MULTIPLE-MYELOMA CELLS INDUCED APOPTOSIS TUMOR-SUPPRESSOR DOWN-REGULATION NECK-CANCER EXPRESSION MICRORNA-29B HEAD ACTIVATION |
| Issue Date | 2014 |
| Publisher | oral oncology |
| Citation | ORAL ONCOLOGY.2014,50,(11),1062-1071. |
| Abstract | Objectives: miR-29b has been implicated in various cancers. However, the role of miR-29b in tongue squamous cell carcinoma (TSCC) remains unclear. This study aimed to investigate the role of miR-29b in TSCC progression. Materials and methods: The expression of miR-29b was analyzed in TSCC tissues and cells. Functional studies were performed in TSCC cells. Real time-PCR, Western blot, cell proliferation, transwell, and dual luciferase reporter assays were performed according to standard procedures. Results: miR-29b was significantly decreased in TSCC specimens and cell lines compared with corresponding normal counterparts. Overexpression of miR-29b significantly inhibited the proliferation, migration, invasion, and cell-cycle progression of TSCC cells, and promoted apoptosis. Moreover, miR-29b targeted the 30 untranslated region of the Sp1 transcript and resulted in the deregulation of Sp1. The inhibition of Sp1 by miR-29b subsequently resulted in the upregulation of PTEN, leading to a decline of phosphorylated AKT. Knockdown of Sp1 in TSCC cell lines mimicked the effects of miR-29b overexpression. In addition, the expression of miR-29b was inversely correlated with Sp1 and positively correlated with the PTEN in TSCC specimens. Conclusion: miR-29b functions as a tumor suppressor in TSCC, and the miR-29b/Sp1/PTEN/AKT axis might represent a potential therapeutic target for TSCC intervention. (C) 2014 Elsevier Ltd. All rights reserved. |
| URI | http://hdl.handle.net/20.500.11897/163007 |
| ISSN | 1368-8375 |
| DOI | 10.1016/j.oraloncology.2014.07.010 |
| Indexed | SCI(E) PubMed |
| Appears in Collections: | 口腔医院 |
