PMID- 22823535 OWN - NLM STAT- MEDLINE DCOM- 20130823 LR - 20181202 IS - 1600-0714 (Electronic) IS - 0904-2512 (Linking) VI - 42 IP - 2 DP - 2013 Feb TI - MicroRNA155 in the growth and invasion of salivary adenoid cystic carcinoma. PG - 140-7 LID - 10.1111/j.1600-0714.2012.01189.x [doi] AB - BACKGROUND: The carcinogenesis mechanism of adenoid cystic carcinoma (ACC) of the salivary gland is poorly understood. MicroRNA155 (miRNA155) has been involved in the carcinogenesis of many malignant tumors. The present study aims to examine the role of miRNA155 in tumor growth and invasion of ACC. METHODS: MiRNA155 expression was determined in ACC specimens along with normal salivary glands by quantitative PCR. Using ACC-2 cells as a model for ACC, cell proliferation was examined by MTT assay after knocking down miRNA155 expression, and cell cycle analysis was performed. Invasive capacity of ACC-2 cells was examined by a Transwell culture assay. The effect of miRNA155 on tumor growth was also examined in vivo using mouse models. The effect of miRNA155 on epidermal growth factor receptor (EGFR)/NF-kappaB was studied by quantitative PCR and electrophoretic mobility shift assay. RESULTS: MiRNA155 was over-expressed in ACC. Proliferation of ACC-2 cells was markedly inhibited by knocking down miRNA155, resulting from a blockade of cell cycle in the G1 phase. Inhibition of miRNA155 significantly suppressed the invasive capacity of ACC-2 cells. In vivo growth of ACC-2 cell-derived tumors was significantly slower by inhibition of miRNA155. Inhibition of miRNA155 also resulted in decreased expression of EGFR and RelA (NF-kappaB). CONCLUSION: The results suggest that miRNA155 facilitates cell cycle progression and promotes invasion in ACC and that the EGFR/NF-kappaB pathway might participate in mediating the effects of miRNA155. This study has provided insights into the carcinogenic mechanisms of ACC and identified new targets for intervention of salivary ACC. CI - (c) 2012 John Wiley & Sons A/S. FAU - Liu, Liu AU - Liu L AD - Department of Oral and Maxillofacial Surgery, School of Stomatology, The 9th People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China. cycstal2004@hotmail.com FAU - Hu, Yongjie AU - Hu Y FAU - Fu, Jingye AU - Fu J FAU - Yang, Xihu AU - Yang X FAU - Zhang, Zhiyuan AU - Zhang Z LA - eng PT - Journal Article DEP - 20120723 PL - Denmark TA - J Oral Pathol Med JT - Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology JID - 8911934 RN - 0 (Coloring Agents) RN - 0 (MIRN155 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (NF-kappa B) RN - 0 (RELA protein, human) RN - 0 (Tetrazolium Salts) RN - 0 (Thiazoles) RN - 0 (Transcription Factor RelA) RN - EC 2.7.10.1 (ErbB Receptors) RN - EUY85H477I (thiazolyl blue) SB - IM MH - Animals MH - Carcinoma, Adenoid Cystic/genetics/*pathology/secondary MH - Cell Cycle MH - Cell Line, Tumor MH - Cell Proliferation MH - Cell Transformation, Neoplastic/pathology MH - Coloring Agents MH - Disease Models, Animal MH - Electrophoretic Mobility Shift Assay MH - ErbB Receptors/analysis MH - Female MH - G1 Phase MH - Gene Expression Regulation, Neoplastic MH - Gene Knockdown Techniques MH - Humans MH - Male MH - Mice MH - Mice, Inbred BALB C MH - MicroRNAs/antagonists & inhibitors/*physiology MH - Middle Aged MH - NF-kappa B/analysis MH - Neoplasm Invasiveness MH - Parotid Gland/pathology MH - Polymerase Chain Reaction MH - Salivary Gland Neoplasms/genetics/*pathology MH - Tetrazolium Salts MH - Thiazoles MH - Transcription Factor RelA/analysis EDAT- 2012/07/25 06:00 MHDA- 2013/08/24 06:00 CRDT- 2012/07/25 06:00 PHST- 2012/07/25 06:00 [entrez] PHST- 2012/07/25 06:00 [pubmed] PHST- 2013/08/24 06:00 [medline] AID - 10.1111/j.1600-0714.2012.01189.x [doi] PST - ppublish SO - J Oral Pathol Med. 2013 Feb;42(2):140-7. doi: 10.1111/j.1600-0714.2012.01189.x. Epub 2012 Jul 23.