RETRACTED: MicroRNA-298 represses hepatocellular carcinoma progression by inhibiting CTNND1-mediated Wnt/β-catenin signaling

Cao, Ningjia; Mao, Liang; Yang, Wei; Liu, Li; Liang, Liang; Zhang, Hong

doi:10.1016/j.biopha.2018.06.135

Cited by 29 publications

(27 citation statements)

References 25 publications

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“…Previous studies have found that miRNAs promote HCC invasion and metastasis via the Wnt/β-catenin signaling pathway (28,29). The results of the present study demonstrated that overexpression of miR-2053 resulted in a reduction in Wnt3 protein levels.…”

Section: Mir-2053 Inhibits Activation Of the Wnt/β-catenin Signaling supporting

confidence: 67%

MicroRNA‑2053 overexpression inhibits the development and progression of hepatocellular carcinoma

Song

Zhao

et al. 2019

Oncol Lett

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MicroRNAs (miRNAs) represent a class of small RNAs that participate in the regulation of tumor progression. However, the identification of functional miRNAs in tumors has not been thoroughly elucidated. In the present study we aim to investigate the impact of altered miR-2053 expression in hepatocellular carcinoma (HCC) cells. The results of the present study demonstrated that miR-2053 overexpression inhibited cell proliferation, migration and invasion, and promoted apoptosis in a HCC cell line, while miR-2053 knockdown induced the opposite cellular phenotypic changes. Mechanistically, it was found that overexpression of miR-2053 resulted in the downregulation of the phosphoinositide 3-kinase (PI3K) and Wnt/β-catenin signaling pathways, which are aberrantly expressed in HCC. Collectively, the results indicate that miR-2053 serves as a tumor suppressor with a crucial role in inhibiting the proliferation, migration and invasion of HCC via targeting the PI3K and Wnt/β-catenin signaling pathways. These data indicate a potential application of miR-2053 in cancer therapy.

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Section: Mir-2053 Inhibits Activation Of the Wnt/β-catenin Signaling supporting

confidence: 67%

MicroRNA‑2053 overexpression inhibits the development and progression of hepatocellular carcinoma

Song

Zhao

et al. 2019

Oncol Lett

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“…The expression of miR-298 in thyroid cancer cells was further tested and a consistent conclusionwas reached. Studies in the past demonstrated that miR-298 exerted oncogene function in some malignant tumors, for example, it could inhibit the progress of hepatocellular carcinoma by inhibiting expression of CTNND1 (14). In order to confirm our hypothesis that miR-298 also played a role in tumor suppressor genes in thyroid cancer, we subsequently overexpressed and underexpressed miR-298 in thyroid cancer cells SW579 and KHm-2 respectively.…”

Section: Discussionmentioning

confidence: 66%

Effects of CDK6 regulated by miR‑298 on proliferation and apoptosis of thyroid cancer cells

Li¹,

Liu²,

Zhao

et al. 2020

Oncol Lett

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Effects of CDK6 regulated by miR-298 on proliferation and apoptosis of thyroid cancer cells were explored. Seventy-five cases of thyroid carcinoma and adjacent tissues were collected. The expression levels of miR-298 and CDK6 mRNA in tissues and cells were detected by RT-PCR. In addition, thyroid cancer cells and human normal thyroid cells Nthy-ori3-1 were purchased, with the former transfected with miR-298-mimics, miR-298-inhibitor, miR-NC, si-CDK6, si-NC, Sh-CDK6, Sh-NC to build cell models. Then the expression levels of miR-298 and CDK6 in thyroid cancer tissues and cells were detected by qRT-PCR, and the expression of CDK6, Bax, Bcl-2 and caspase-3 by WB. CCK-8 and flow cytometry were employed to detect cell proliferation and apoptosis, and dual luciferase report was adopted to determine the relationship between miR-298 and CDK6. miR-298 was underexpressed in thyroid cancer, and CDK6 was highly expressed in thyroid cancer. Cell experiments revealed that overexpression of miR-298 or inhibition of CDK6 expression could suppress cell proliferation, promote apoptosis, and significantly increase the expression levels of Bax and caspase-3 proteins, decrease Bcl-2 protein expression, which was contrary to the biological phenotype of cells after inhibition of miR-298 or further overexpression of CDK6. Dual luciferase report confirmed that miR-298 was a targeting site of CDK6. miR-298 can inhibit the proliferation of thyroid cells and promote apoptosis of thyroid cancer cells by regulating the expression of CDK6, which is expected to be a potential target for clinical application.

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“…A large amount of recent data has implicated CTNND1 in the regulation of cancer development and progression 35,47 , and previous studies have demonstrated that CTNND1 plays a functional role in HCC cell proliferation, migration, invasion, and metastasis. CTNND1 overexpression in HCC cells has been shown to induce epithelial-to-mesenchymal transition, migration, and invasion in vitro and also to enhance the metastatic potential in vivo 48,49 . While our data are consistent with those of these previous studies, we additionally revealed that circMAST1-miR-1299 regulates CTNND1 as part of a sponging mechanism.…”

Section: Discussionmentioning

confidence: 99%

The circular RNA circMAST1 promotes hepatocellular carcinoma cell proliferation and migration by sponging miR-1299 and regulating CTNND1 expression

Sheng

Sun

et al. 2020

Cell Death Dis

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Circular RNAs (circRNAs) are a class of non-coding RNAs with a loop structure; however, their functions remain largely unknown. Growing evidence suggests that circRNAs play a pivotal role in the progression of malignant diseases. However, the expression profiles and function of circRNAs in hepatocellular carcinoma (HCC) remain unclear. We investigated the expression of microtubule-associated serine/threonine kinase 1 (MAST1) circRNA (circMAST1) in HCC and healthy tissues using bioinformatics, quantitative real-time PCR (qRT-PCR), and fluorescence in situ hybridization. Luciferase reporter assays were performed to assess the interaction between circMAST1 and miR-1299. Proliferation assays, colony formation assays, flow cytometry, transwell assays, and western blotting were also performed. A mouse xenograft model was also used to determine the effect of circMAST1 on HCC growth in vivo. CircMAST1 was upregulated in HCC tissues and cell lines; silencing via small interfering RNA inhibited migration, invasion, and proliferation of HCC cell lines in vitro as well as tumor growth in vivo. Furthermore, the expression of circMAST1 was positively correlated with catenin delta-1 (CTNND1) and negatively correlated with microRNA (miR)-1299 in HCC clinical samples. Importantly, circMAST1 sponged miR-1299 to stabilize the expression of CTNND1 and promoted tumorigenic features in HCC cell lines. We found that circMAST1 may serve as a novel biomarker for HCC. Moreover, circMAST1 elicits HCC progression by sponging miRNA-1299 and stabilizing CTNND1. Our data provide potential options for therapeutic targets in patients with HCC.

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RETRACTED: MicroRNA-298 represses hepatocellular carcinoma progression by inhibiting CTNND1-mediated Wnt/β-catenin signaling

Cited by 29 publications

References 25 publications

MicroRNA‑2053 overexpression inhibits the development and progression of hepatocellular carcinoma

MicroRNA‑2053 overexpression inhibits the development and progression of hepatocellular carcinoma

Effects of CDK6 regulated by miR‑298 on proliferation and apoptosis of thyroid cancer cells

The circular RNA circMAST1 promotes hepatocellular carcinoma cell proliferation and migration by sponging miR-1299 and regulating CTNND1 expression

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