Thumbnail
Access Restriction
Open

Author Zhang, Chen-Zheng
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ ANIMAL TISSUES ♦ ANTIGENS ♦ CARCINOMAS ♦ CELL PROLIFERATION ♦ DIAGNOSIS ♦ IN VIVO ♦ INHIBITION ♦ ONCOGENES ♦ RNA ♦ THERAPY
Abstract Recently, long noncoding RNAs (lncRNAs) have been reported to have crucial regulatory efficiency in human cancer biology. Long intergenic non-coding RNA 668 (LINC00668) was regarded as an oncogene in multiple cancers. However, the underlying molecular mechanism of LINC00668 in oral squamous cell carcinoma (OSCC) has not been studied. In this study, we first demonstrated that LINC00668 expression was up-regulated, which was correlated with tumor progression, and miR-297 down-regulated in OSCC tissues and cells. Importantly, LINC00668 expression was negatively correlated with miR-297 expression in OSCC tissues. Loss-of-function of LINC00668 revealed that LINC00668 functioned as a ceRNA for miR-297 to facilitate VEGFA expression, promoting OSCC progression. Furthermore, LINC00668 knockdown suppressed tumor growth and reduced the expression of proliferation antigen ki-67 in vivo. Finally, we confirmed that LINC00668 promoted OSCC activity through VEGFA signaling. In conclusion, these results suggest that LINC00668 promotes OSCC tumorigenesis via miR-297/VEGFA axis, which may provide a new target for the diagnosis and therapy of OSCC disease. - Highlights: • LINC00668 is up-regulated in human primary OSCC tissues. • Expression of VEGFA is up-regulated in primary human OSCC and negatively expressed related to miR-297. • miR-297 inhibits the tumorigenic potential of OSCC cells by down-regulating oncogenic VEGFA gene. • LINC00668's oncogenic functions are partially through reverse regulation of miRNA-297, and then activation of VEGFA.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2017-08-05
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 489
Issue Number 4


Open content in new tab

   Open content in new tab