RETRACTED: ANRIL acts as onco-lncRNA by regulation of microRNA-24/c-Myc, MEK/ERK and Wnt/β-catenin pathway in retinoblastoma

Yu, Feifei; Pang, Guolong; Zhao, Guopeng

doi:10.1016/j.ijbiomac.2019.01.157

Cited by 28 publications

(17 citation statements)

References 39 publications

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“…Furthermore, lncRNA could modulate gene location . Additionally, it has been shown that lncRNA ANRIL acts as a ceRNA to sponging miR‐181a, miR‐24, and miR‐125a‐3p . These effects indicate that ANRIL functions distinctively in different tumors or diseases.…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA ANRIL enhances mitochondrial function of hepatocellular carcinoma by regulating the MiR‐199a‐5p/ARL2 axis

Bao

Wei

et al. 2019

Environmental Toxicology

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Although the roles of long non-coding RNA (lncRNA) ANRIL (Antisense non-coding RNA in the INK4A locus) have been established in various tumors, its roles in mitochondrial metabolic reprogramming of hepatocellular carcinoma (HCC) cells are still unclear. This work aims to explore lncRNA ANRIL roles in regulating the mitochondrial metabolic reprogramming of liver cancer cells. First, we found that lncRAN ANRIL expression was significantly increased in HCC tissues or cells compared with the normal adjacent tissues and normal tissues or cells. Functional experiment showed that overexpression of lncRNA ANRIL promoted mitochondrial function in HCC cells, evident by the increased mitochondrial DNA copy numbers, ATP (Adenosine triphosphate) level, mitochondrial membrane potential, and the expression levels of mitochondrial markers, while ANRIL knockdown exerted the opposite effects. Mechanistically, lncRNA ANRIL acted as a competing endogenous RNA to increase ARL2 (ADP-ribosylationfactor-like 2) expression via sponging miR-199a-5p. Notably, the miR-199a-5p/ARL2 axis is necessary for ANRIL-mediated promoting effects on HCC cell mitochondrial function. This work reveals a novel ANRIL-miR-199a-5p-ARL2 axis in HCC cell progression, which might provide potential targets for HCC treatment. K E Y W O R D SANRIL, ARL2, ceRNA, hepatocellular carcinoma, lncRNA, miR-199a-5p

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Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA ANRIL enhances mitochondrial function of hepatocellular carcinoma by regulating the MiR‐199a‐5p/ARL2 axis

Bao

Wei

et al. 2019

Environmental Toxicology

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“…18,19 Several studies demonstrated that CDKN2B-AS1 sponges different miRNAs to modulate tumor progression, such as miR-181a-5p, miR-125a-3p, miR-24, miR-191, miR-122-5p, miR-34a, and miR-199a. [24][25][26][27][28][29][30] In our study, we identified that miR-497 could bind with CDKN2B-AS1 through a public database (Starbase 2.0). Then, luciferase reporter and RIP assays confirmed that CDKN2B-AS1 could specifically associate with miR-497 in LSCC cells.…”

Section: Dovepressmentioning

confidence: 99%

<p>Long Non-Coding RNA CDKN2B-AS1 Facilitates Laryngeal Squamous Cell Cancer Through Regulating miR-497/CDK6 Pathway</p>

Cui¹,

Yu²,

Shang³

et al. 2019

OTT

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Background: CDKN2B antisense RNA 1 (CDKN2B-AS1), a long noncoding RNA, was reported to play crucial roles in the progression of multiple cancers. However, the functional roles and regulatory mechanism of CDKN2B-AS1 in human laryngeal squamous cell cancer (LSCC) remain unclear. The goals of this study were to investigate biological roles and underlying mechanisms of CDKN2B-AS1 in LSCC. Methods: The expressions of CDKN2B-AS1, miR-497 and cyclin-dependent kinase 6 (CDK6) were detected in LSCC tissues and cell lines by real-time quantitative PCR (qRT-PCR). The effects of CDKN2B-AS1 on LSCC cell proliferation, apoptosis, migration and invasion were examined by corresponding experiments. Bioinformatics analysis and luciferase activity assay were applied to analyze the interaction between CDKN2B-AS1 and miR-497. Results: The expression of CDKN2B-AS1 was significantly higher in LSCC tissues than in adjacent normal tissues. Higher CDKN2B-AS1 was closely associated with lymph node metastasis and advanced clinical stage. Moreover, CDKN2B-AS1 knockdown by siRNA significantly inhibited the proliferation, induced cell apoptosis, and suppressed migration and invasion in LSCC cells. Mechanically, CDKN2B functions as an oncogenic lncRNA in LSCC via regulating miR-497/CDK6 axis. Conclusion: The observations in this study identify CDKN2B-AS1 an oncogenic role in the tumorigenesis of LSCC by regulating miR-497/CDK6 axis and indicate that it may serve as a potential target for LSCC treatment.

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“…The MeK/erK pathway regulates a number of important cellular functions including proliferation, differentiation, survival and migration (27). Previous studies have demonstrated that over-activation of MeK/erK signaling is involved in the oncogenesis of human cancers, which makes it an appealing target for anticancer therapeutics (28)(29)(30)(31). The MeK/erK pathway serves important roles in regulating gastric cancer (29), retinoblastoma (30) and pancreatic cancer (31) oncogenesis.…”

Section: Discussionmentioning

confidence: 99%

LncRNA HOTTIP promotes the proliferation and invasion of ovarian cancer cells by activating the MEK/ERK pathway

Liu

et al. 2020

Mol Med Rep

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recent studies have revealed that long non-coding rnas (lncrnas) serve important roles in carcinogenesis and that this type of gene may be used as biomarkers in cancer. a high level of lncrna HoXa distal transcript antisense rna (HoTTiP) is associated with unfavorable prognosis for patients with ovarian cancer (oc), but the mechanism of HoTTiP involved in oc development remains to be elucidated. The present study aimed to investigate the mechanism of HoTTiP in metastasis-associated oc cell behaviors. HoTTiP levels in ovarian cells were quantified by reverse transcription-quantitative Pcr, cell proliferation was analyzed by colony formation assay, and apoptosis was assessed by flow cytometry. Cell migratory and invasive abilities were evaluated by wound healing and Transwell assays, respectively. The expression levels of mitogen-activated protein kinase kinase (MeK)/erK pathway-associated proteins were detected by western blotting. The results demonstrated that knockdown of HoTTiP in OC cells significantly reduced the phosphorylation levels of MeK and erK, inhibited the proliferation and invasion of oc cells and promoted their apoptosis. Furthermore, the effects of HoTTiP on cell migration and invasion were partly associated with the epithelial-mesenchymal transition (eMT) process. Proliferation, invasion and eMT of oc cells were enhanced following overexpression of HoTTiP; however, these effects were reversed by the MeK/erK pathway inhibitor u0126. in conclusion, HoTTiP was demonstrated to promote the proliferation, migration and invasion of oc cells by activating the MeK/erK pathway. Therefore, HoTTiP may serve as a potential therapeutic target for oc.

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RETRACTED: ANRIL acts as onco-lncRNA by regulation of microRNA-24/c-Myc, MEK/ERK and Wnt/β-catenin pathway in retinoblastoma

Cited by 28 publications

References 39 publications

Long non‐coding RNA ANRIL enhances mitochondrial function of hepatocellular carcinoma by regulating the MiR‐199a‐5p/ARL2 axis

Long non‐coding RNA ANRIL enhances mitochondrial function of hepatocellular carcinoma by regulating the MiR‐199a‐5p/ARL2 axis

<p>Long Non-Coding RNA CDKN2B-AS1 Facilitates Laryngeal Squamous Cell Cancer Through Regulating miR-497/CDK6 Pathway</p>

LncRNA HOTTIP promotes the proliferation and invasion of ovarian cancer cells by activating the MEK/ERK pathway

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