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Retracted : Long non‐coding RNA LINC00152 promotes cell growth and invasion of papillary thyroid carcinoma by regulating the miR‐497/BDNF axis
Author(s) -
Sun Zhihui,
Guo Xun,
Zang Mingcui,
Wang Peisong,
Xue Shuai,
Chen Guang
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.26928
Subject(s) - cell growth , gene knockdown , cancer research , carcinogenesis , biology , thyroid carcinoma , cell migration , long non coding rna , thyroid cancer , cell culture , cell , microbiology and biotechnology , rna , cancer , endocrinology , thyroid , biochemistry , gene , genetics
Long intergenic non‐coding RNA 152 (LINC00152) was reported to be tightly linked to tumorigenesis and progression in multiple cancers. However, its biological role and modulatory mechanism in papillary thyroid carcinoma (PTC) has not been elucidated. In this study, we determined the expression levels of LINC00152 in PTC tissues and cell lines by quantitative real time polymerase chain reaction (qRT‐PCR). Cell proliferation, colony formation, migration, and invasion were measured by a Cell Counting Kit‐8 assay, colony formation analysis, wound healing, and transwell invasion assay, respectively. A luciferase reporter assay and qRT‐PCR were used to determine whether LINC00152 interacts with miR‐497 directly. We established a xenograft mouse model to examine the underlying molecular mechanism and effect of LINC00152 on tumor growth in vivo. We found that LINC00152 expression was significantly increased in PTC tissues and derived cell lines. LINC00152 knockdown significantly inhibited proliferation, colony formation, migration, and invasion in vitro, and impaired tumor growth in vivo. We revealed that LINC00152 functioned as a competing endogenous RNA to the miR‐497 sponge, downregulating its downstream target brain‐derived neurotrophic factor (BDNF), which is an oncogene in thyroid cancer. These findings suggest that LINC00152 is responsible for PTC cell proliferation and invasion and exerts its function by regulating the miR‐497/BDNF axis.