Downregulation of lncRNA OGFRP1 inhibits hepatocellular carcinoma progression by AKT/mTOR and Wnt/&amp;beta;-catenin signaling pathways

Chen, Wei; You, Jia; Zheng, Qi; Zhu, Yueyong

doi:10.2147/cmar.s164911

Cited by 41 publications

(39 citation statements)

References 44 publications

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“…Aberrant activation of this pathway occurs in many malignant tumours including endometrial cancer [17,37]. In addition, the downregulation of OGFRP1 has been revealed to inhibit hepatocellular carcinoma via the regulation of AKT/mTOR and Wnt/b-catenin signals [19]. Koga et al pointed out that the PI3K/AKT/GSK-3b signals is crucial to SIRT1 induction by stress reaction of endoplasmic reticulum and consequently regulates hepatocellular injury [38].…”

Section: Discussionmentioning

confidence: 99%

“…A recent study has shown that lncRNA DLEU1 enhances the progression of endometrial cancer through activation of PI3K/AKT/GSK-3b pathway [18]. Moreover, OGFRP1 downregulation was shown to inhibit hepatocellular carcinoma by regulating AKT/mTOR and Wnt/b-catenin signals [19]. We investigated whether activation of PI3K/AKT/GSK-3b pathway is a key mechanism that mediates the role of OGFRP1 in endometrial cancer.…”

Section: R E T R a C T E Dmentioning

confidence: 99%

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RETRACTED ARTICLE: Upregulation of long non-coding RNA OGFRP1 facilitates endometrial cancer through regulating miR-124-3p/SIRT1 axis and activating PI3K/AKT/GSK-3β pathway

Chen

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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We planned to investigate the possible influences of long non-coding RNA (opioid growth factor receptor pseudogene 1) OGFRP1 in endometrial cancer and its potential regulatory mechanism. We measured the level of OGFRP1 in endometrial cancer tissues and evaluated the influences of OGFRP1 dysregulation on the tumour cell biological processes of endometrial cancer cells. Further, the regulatory relationships between OGFRP1 and miR-124-3p, between miR-124-3p and Sirtuin1 (SIRT1) were, respectively, investigated. The interaction between OGFRP1 dysregulation and activation of PI3K/AKT/ GSK-3b pathway was revealed by Western blotting. OGFRP1 was up-regulated in endometrial cancer tissues and cells. OGFRP1 suppression inhibited the malignant behaviour (inhibited cell viability, promoted cell apoptosis, and suppressed cell migration and invasion) of the Ishikawa cells via negatively regulating miR-124-3p. SIRT1 was a target gene of miR-124-3p, and miR-124-3p regulated tumour growth and metastasis by the downstream signal of SIRT1. Moreover, suppression of OGFRP1 restrained the activation of PI3K/AKT/GSK-3b signals in the Ishikawa cells via miR-124-3p/SIRT1 axis. Our experiments revealed that upregulation of OGFRP1 may enhance the progression of endometrial cancer by regulating miR-124-3p/SIRT1 axis and by activating PI3K/AKT/GSK-3b pathway. OGFRP1 may be of significance in illustrating the biology of endometrial cancer.

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Section: Discussionmentioning

confidence: 99%

Section: R E T R a C T E Dmentioning

confidence: 99%

RETRACTED ARTICLE: Upregulation of long non-coding RNA OGFRP1 facilitates endometrial cancer through regulating miR-124-3p/SIRT1 axis and activating PI3K/AKT/GSK-3β pathway

Chen

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Interestingly, studies have shown that activated AKT could result in phosphorylation and inactivation of GSK3β [13,14], which therefore promotes β-catenin accumulation and nuclear translocation in Wnt/β-catenin pathway [15]. These previous findings indicate the crosstalk between AKT/mTOR and Wnt/β-catenin signaling pathways, and the regulation of these two pathways has also been reported in several cancers [16,17]. Although both AKT/mTOR and Wnt/β-catenin pathways have been investigated in cervical cancer respectively [18,19], no studies have been reported on the regulation of these pathways by GHET1 in CC.…”

Section: Introductionmentioning

confidence: 76%

LncRNA GHET1 promotes cervical cancer progression through regulating AKT/mTOR and Wnt/β-catenin signaling pathways

Liu

Luo

et al. 2020

Bioscience Reports

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Cervical cancer (CC) is a prevalent gynecological cancer, and the patients with CC usually suffer from dismal prognosis. Long non-coding RNAs (lncRNAs) are demonstrated to serve as promising biological targets in human cancers. Gastric carcinoma proliferation enhancing transcript 1 (GHET1) has been revealed to function as an oncogene in several cancers, but it has never been investigated in CC. We proposed to examine the biological role of GHET1 in CC and the underlying mechanism and validated the up-regulated expression of GHET1 in CC cell lines. Loss-of-function assays demonstrated that down-regulation of GHET1 inhibited cell growth, migration and epithelial-to-mesenchymal transition (EMT) in CC. Furthermore, we validated that GHET1 down-regulation could inactivate AKT/mTOR and Wnt/β-catenin pathways, and that respective activation of these two pathways abrogated the inhibitive effect of GHET1 knockdown on CC cell growth, migration and EMT. Moreover, we unfolded a preliminary investigation on the modulation of GHET1 on AKT/mTOR and Wnt/β-catenin pathways. We found that GHET1 stabilized E2F6 mRNA through interacting with IGF2BP2, so as to regulate the activity of AKT/mTOR and Wnt/β-catenin pathways. Rescue assays also proved that GHET1 regulated these two pathways and CC cell growth, migration and EMT through E2F6. In conclusion, we revealed that down-regulation of GHET1 suppresses cervical cancer progression through regulating AKT/mTOR and Wnt/β-catenin signaling pathways, indicating GHET1 as a promising molecular biomarker for CC treatment improvement.

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“…. For example, downregulation of lncRNA OGFRP1 can inhibit HCC progression through AKT/mTOR signaling (Chen, You, Zheng, & Zhu, 2018). PTTG3P promotes HCC progression via upregulating PTTG1 and PI3K/AKT (Huang et al, 2018).…”

mentioning

confidence: 99%

DANCR contributed to hepatocellular carcinoma malignancy via sponging miR‐216a‐5p and modulating KLF12

Wang

Zhang

et al. 2018

Journal Cellular Physiology

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Long noncoding RNA (lncRNA) differentiation antagonizing nonprotein coding RNA (DANCR) has been identified as an oncogene in several cancers. However, the biological function and role of DANCR in hepatocellular carcinoma (HCC) remain unclear. Our current study aimed to investigate the detailed mechanism of DANCR in HCC. We found that DANCR was significantly upregulated in HCC cell lines in comparison to LO2 cells. Then, we observed that knockdown of DANCR could greatly inhibit Huh7 and HepG2 cell proliferation. In addition, HCC cell apoptosis was increased by silence of DANCR and meanwhile, cell cycle progression was blocked in G1 phase. Apart from these, downregulation of DANCR repressed HCC cell migration and invasion ability obviously. As predicted by the bioinformatics analysis, microRNA‐216a‐5p (miR‐216a‐5p) could serve as a direct target of DANCR. MiR‐216a‐5p has been reported to be involved in many cancers. Here, the correlation between miR‐216a‐5p and DANCR was confirmed using dual‐luciferase reporter assay and radioimmunoprecipitation assay. Subsequently, Kruppel‐like factor 12 (KLF12) exerts an important role in different tumor types. KLF12 can function as a downstream target of miR‐216a‐5p. Finally, the in vivo experiments were used and the data proved that DANCR also strongly suppressed HCC tumor growth in vivo via targeting miR‐216a‐5p and KLF12. In conclusion, our study indicated that DANCR might provide a new perspective for HCC treatment.

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Downregulation of lncRNA OGFRP1 inhibits hepatocellular carcinoma progression by AKT/mTOR and Wnt/β-catenin signaling pathways

Cited by 41 publications

References 44 publications

RETRACTED ARTICLE: Upregulation of long non-coding RNA OGFRP1 facilitates endometrial cancer through regulating miR-124-3p/SIRT1 axis and activating PI3K/AKT/GSK-3β pathway

RETRACTED ARTICLE: Upregulation of long non-coding RNA OGFRP1 facilitates endometrial cancer through regulating miR-124-3p/SIRT1 axis and activating PI3K/AKT/GSK-3β pathway

LncRNA GHET1 promotes cervical cancer progression through regulating AKT/mTOR and Wnt/β-catenin signaling pathways

DANCR contributed to hepatocellular carcinoma malignancy via sponging miR‐216a‐5p and modulating KLF12

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