Circular RNA circGFRA1 promotes angiogenesis, cell proliferation and migration of hepatocellular carcinoma by combining with miR-149.

OBJECTIVE: We aimed to explore the effect of circGFRA1 on the progression of hepatocellular carcinoma (HCC) and its underlying mechanism. PATIENTS AND METHODS: First, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was conducted to detect the level of circGFRA1 in HCC tissues and cells. Survival analysis was applied to detect the effect of highly expressed circGFRA1 on the prognosis of HCC patients. Subsequently, circGFRA1 level was silenced in HCC cells, and proliferative, migration and angiogenesis activity of HCC cells was examined using Cell Counting Kit-8 (CCK-8), transwell test, and angiogenesis experiment. Then, we predicted the binding target of circGFRA1 through the bioinformatics website, and verified it through qRT-PCR and Dual-Luciferase reporter assay. Lastly, the interaction between them was verified through a series of in vitro experiments. RESULTS: qRT-PCR analysis showed that circGFRA1 was abnormally highly expressed in HCC tissues and HCC cells, and the high expression of circGFRA1 may lead to poor prognosis in patients with HCC. After transfecting si-circGFRA1 in HCC cells, CCK-8 and transwell experiments showed that the proliferative ability and migration of HCC cells were inhibited. Moreover, angiogenesis experiments showed that the knockdown of circGFRA1 can inhibit the blood vessels replenishment of HCC cells. The bioinformatics website suggested that miR-149 may be able to bind circGFRA1. MiR-149 was upregulated by the knockdown of circGFRA1 in HCC cells. Pearson analysis suggested that the expression levels of the two genes were negatively correlated. Dual-Luciferase reporter assay further indicated that circGFRA1 can bind to miR-149. Reverse experiment showed that the knockdown of miR-149 can partially restore the inhibited proliferative, migration, and angiogenesis activity of HCC cells caused by circGFRA1 knockdown. CONCLUSIONS: CircGFRA1 is highly expressed in HCC and its level is negatively correlated with miR-149 expression. CircGFRA1 can promote the proliferative, migration and angiogenic activity of HCC by binding miR-149.

Long non-coding RNA NEAT1 promotes tumor development and metastasis through targeting miR-224-5p in malignant melanoma.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long non-coding RNA NEAT1 promotes tumor development and metastasis through targeting miR-224-5p in malignant melanoma, by J.-X. Zou, T.-W. Ge, published in Eur Rev Med Pharmacol Sci 2020; 24 (3): 1302-1308-DOI: 10.26355/eurrev_202002_20187-PMID: 32096166" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/20187.

Long non-coding RNA NEAT1 promotes tumor development and metastasis through targeting miR-224-5p in malignant melanoma.

OBJECTIVE: Melanoma is one of the most ordinary malignant tumors. Recent studies have revealed that long noncoding RNAs (lncRNAs) play an important role in the progression of tumorigenesis. This work aims to identify how lncRNA NEAT1 functions in the progression of melanoma. PATIENTS AND METHODS: NEAT1 expression of both melanoma patients' tissue samples and cell lines was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the function of NEAT1 was identified by performing the proliferation and transwell assay in vitro. Besides, the underlying mechanism was explored through the Luciferase assay and RNA immunoprecipitation (RIP) assay. In addition, tumor formation and metastasis assays were also conducted in vivo. RESULTS: In this research, NEAT1 expression was significantly higher in melanoma tissues compared with that in skin tissues with the melanocytic nevus. Cell proliferation and invasion of melanoma were inhibited after the knockdown of NEAT1 in vitro. Moreover, the results of further experiments revealed that microRNA-224-5p (miR-224-5p) was upregulated via the knockdown of NEAT1 and was also a direct target of NEAT1 in melanoma. Furthermore, tumor formation and metastasis of melanoma were inhibited via the knockdown of NEAT1 in nude mice. CONCLUSIONS: Our study suggests that NEAT1 enhances melanoma cell proliferation and metastasis via sponging miR-224-5p in vitro and in vivo.