Abstract:
:The incidence of oral squamous cell carcinoma (OSCC) is continuously increasing while its survival rate has not notably improved. There is a pressing need for improved understanding of the genetic regulation of OSCC tumorigenesis and progression. In this study, the function of miR-448 in the regulation of OSCC growth and its putative target were thoroughly analyzed in vitro. The expression of miR-448 was detected in human OSCC specimens and OSCC cell lines (Cal-27 and Scc-9) by reverse transcription-quantitative polymerase chain reaction. The function of miR-448 was investigated in Cal-27 cells transfected with miR-448 inhibitor, and its putative target determined using a luciferase reporter assay. MTT and wound healing assays and flow cytometry were used to evaluate the effects of miR-448 on OSCC proliferation, metastasis and apoptosis. The level of miR-448 was significantly elevated in human OSCC tissues and the Cal-27 cell line. Suppression of miR-448 expression attenuated cell proliferation and migration, and induced apoptosis of Cal-27 cells. Furthermore, miR-448 bound with the 3'-untranslated region of metallophosphoesterase domain containing 2 (MPPED2) mRNA, thereby reducing the MPPED2 protein level. Thus, it appears that miR-448 acts as a tumor inducer, causing OSCC growth by inhibiting the expression of its target MPPED2. These results demonstrate that miR-448 plays a critical role in OSCC tumorigenesis, and is a potential therapeutic target.
journal_name
Exp Ther Medjournal_title
Experimental and therapeutic medicineauthors
Shen L,Liu L,Ge L,Xie L,Liu S,Sang L,Zhan T,Li Hdoi
10.3892/etm.2016.3659subject
Has Abstractpub_date
2016-10-01 00:00:00pages
2747-2752issue
4eissn
1792-0981issn
1792-1015pii
ETM-0-0-3659journal_volume
12pub_type
杂志文章abstract::Valvular heart disease (VHD) is caused by either damage or defect in one of the four heart valves, aortic, mitral, tricuspid or pulmonary. Defects in these valves can be congenital or acquired. Age, gender, tobacco use, hypercholesterolemia, hypertension, and type II diabetes contribute to the risk of disease. VHD is ...
journal_title:Experimental and therapeutic medicine
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doi:10.3892/etm.2016.3048
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
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doi:10.3892/etm.2016.3296
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journal_title:Experimental and therapeutic medicine
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doi:10.3892/etm.2012.637
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doi:10.3892/etm.2018.6058
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journal_title:Experimental and therapeutic medicine
pub_type: 杂志文章
doi:10.3892/etm.2010.169
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
pub_type: 杂志文章
doi:10.3892/etm.2011.220
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
pub_type: 杂志文章
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journal_title:Experimental and therapeutic medicine
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pub_type: 杂志文章,评审
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
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journal_title:Experimental and therapeutic medicine
pub_type: 杂志文章
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journal_title:Experimental and therapeutic medicine
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更新日期:2019-08-01 00:00:00
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journal_title:Experimental and therapeutic medicine
pub_type: 杂志文章
doi:10.3892/etm.2015.2509
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