Retracted: Long non‐coding RNA LINC00152 promotes cell growth and invasion of papillary thyroid carcinoma by regulating the miR‐497/BDNF axis

Abstract

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.

Long non-coding RNA LINC00152 regulates cell proliferation and migration by epigenetically repressing LRIG1 expression in cholangiocarcinoma

“…In our present study, publicly available data and qRT-PCR results both uncovered that LINC00152 expression in CCA tissues was observably higher than that in corresponding non-tumor tissues, which implied the important role of LINC00152 in CCA progression. LINC00152 was reported upregulated in various cancers, promoting cancer cell proliferation and migration [20][21][22][23][24][25][26][27][28][29][30][31][32]. Nevertheless, the possible role of LINC00152 in CCA is still undocumented.…”

“…Long intergenic non-coding RNA 152 (LINC00152), a 828-bp lncRNA that maps to chromosome 2p11.2, was initially found to be differentially hypomethylated in hepatocarcinogenesis [19]. Continuously, LINC00152 have exhibited carcinogenic properties in a variety of cancers, including gastric cancer, hepatocellular carcinoma, colon cancer, gallbladder cancer, lung adenocarcinoma, breast cancer, nonsmall-cell lung cancer, papillary thyroid carcinoma, tongue squamous cell carcinoma, glioblastoma and ovarian cancer [20][21][22][23][24][25][26][27][28][29][30][31][32]. However, the expression pattern, biological function, and underlying mechanism of LINC00152 in human CCA remain largely unknown.…”

Regulation of microRNA‑497 expression in human cancer (Review)

“…The lncRNA LINC00152, which is located in human Chr2p11.2, is reported to be upregulated in several types of cancer. In thyroid cancer, LINC00152 acts as a miR-497 'sponge', downregulating its downstream target, brain-derived neurotrophic factor (BDNF), to promote the proliferation and invasion of papillary thyroid cancer cells (71). In multiple myeloma, LINC00152 acts as an oncogene and regulates cell growth by targeting miR-497 expression (72).…”

Long noncoding RNA DLX6-AS1 promotes neuroblastoma progression by regulating miR-107/BDNF pathway

“…Recently, accumulating articles revealed that one potential function of lncRNAs was to directly interact with miRNAs as a sponge and regulate their expression and activity [10]. For example, LINC00152 promotes cell growth and invasion of papillary thyroid carcinoma by regulating the miR‐497/BDNF axis [11]. However, the functions of lncRNA on miRNAs in the pathogenesis of NB has not been described.…”