LncRNA AIRN influences the proliferation and apoptosis of hepatocellular carcinoma cells by regulating STAT1 ubiquitination

Cai, Huajie; Zheng, Yijing; Wen, Zhengde; Yang, Yajun; Yang, Shouzhang; Zhang, Qiyu

doi:10.1007/s12272-021-01317-7

Cited by 30 publications

(7 citation statements)

References 34 publications

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“…Airn knockdown reduces the survival of cardiomyocytes under cellular stress and enhances apoptosis. In hepatocellular carcinoma (HCC), Airn is highly expressed and its knockdown inhibits the progression of HCC by restraining cell proliferation and promoting apoptosis [ 32 ]. Decreased Airn expression is reported in diabetic nephropathy, thus leading to decreased cell viability and increased apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…The lncRNA-Airn is imprinted paternally and is located in the antisense orientation to the imprinted insulin growth factor 2 receptor (Igf2r) gene on chromosome 17; thus it regulates the expression of the protein-coding genes in its vicinity, including Igf2r, Slc22a2, and Slc22a3 [27][28][29][30]. Airn is reportedly associated with the development of several diseases, such as hepatocellular carcinoma, alcoholic fatty liver disease, breast cancer, and diabetic nephropathy as it can regulate cellular apoptosis, migration, and mitophagy [31][32][33][34]. Additionally, Airn binds to IMP2, thus controlling the translation of several genes involved in myocardial infarction.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA Airn alleviates diabetic cardiac fibrosis by inhibiting activation of cardiac fibroblasts via a m6A-IMP2-p53 axis

Peng

Liu²,

Hu³

et al. 2022

Biol Direct

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Background Cardiac fibrosis is a leading cause of cardiac dysfunction in patients with diabetes. However, the underlying mechanisms of cardiac fibrosis remain unclear. This study aimed to investigate the role of the long non-coding RNA (LncRNA) Airn in the pathogenesis of cardiac fibrosis in diabetic cardiomyopathy (DCM) and its underlying mechanism. Methods Diabetes mellitus (DM) was induced in mice by streptozotocin injection. An intramyocardial adeno-associated virus (AAV) was used to manipulate Airn expression. The functional significance and underlying mechanisms in DCM fibrosis were investigated both in vitro and in vivo. Results Diabetic hearts showed a significant impairment in cardiac function, accompanied by obviously increased cardiac fibrosis. Interestingly, lncRNA Airn expression was significantly decreased in both diabetic hearts and high glucose (HG)-treated cardiac fibroblasts (CFs). AAV-mediated Airn reconstitution prevented cardiac fibrosis and the development of DCM, while Airn knockdown induced cardiac fibrosis phenotyping DCM. As in vitro, Airn reversed HG-induced fibroblast-myofibroblast transition, aberrant CFs proliferation and section of collagen I. In contrast, Airn knockdown mimicked a HG-induced CFs phenotype. Mechanistically, we identified that Airn exerts anti-fibrotic effects by directly binding to insulin-like growth factor 2 mRNA-binding protein 2 (IMP2) and further prevents its ubiquitination-dependent degradation. Moreover, we revealed that Airn/IMP2 protected p53 mRNA from degradation in m6A manner, leading to CF cell cycle arrest and reduced cardiac fibrosis. As a result, ablation of p53 blunted the inhibitory effects of Airn on fibroblast activation and cardiac fibrosis. Conclusions Our study demonstrated for the first time that Airn prevented the development of cardiac fibrosis in diabetic heart via IMP2-p53 axis in an m6A dependent manner. LncRNA Airn could be a promising therapeutic target for cardiac fibrosis in DCM. Graphical abstract

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

LncRNA Airn alleviates diabetic cardiac fibrosis by inhibiting activation of cardiac fibroblasts via a m6A-IMP2-p53 axis

Peng

Liu²,

Hu³

et al. 2022

Biol Direct

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“…Many studies have demonstrated that lncRNAs can act as key regulators to affect tumor invasion and metastasis [29][30][31], tumor cell proliferation and apoptosis [32][33][34][35],tumor angiogenesis [34,[36][37][38] and regulate tumor drug resistance [39,40]. More and more studies have shown that abnormally expressed lncRNAs are key factors in cancer detection and can be used as non-invasive tumor markers to play an irreplaceable role in the early diagnosis of hepatocellular carcinoma [7,[41][42][43].…”

Section: Discussionmentioning

confidence: 99%

Necroptosis-related lncRNAs and Hepatocellular Carcinoma Undoubtedly Secret

Ning

Sun

Fan

et al. 2022

Preprint

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Background: The current study demonstrates that necroptosis is an important mechanism of carcinogenesis. However, the predictive value of necroptosis-associated long non-coding RNAs (LncRNAs) in hepatocellular carcinoma has not been demonstrated. The purpose of this study is to apply necroptosis-related lncRNAs to construct a predictive signature to predict the prognosis of hepatocellular carcinoma patients.Methods: The clinical and RNA-seq data were downloaded using The Cancer Genome Atlas (TCGA) database. Univariate and multivariate Cox analysis was used to screen out suitable necroptosis-related lncRNAs, and then predictive signature was constructed. The TCGA data were randomly divided into high- and low-risk groups, and the Kaplan-Meier method was used to analyze the overall survival (OS) of the two groups to verify the predictive signature. Finally, a prognostic correlation model for predicting disease-freesurvival （DFS）in hepatocellular carcinoma（HCC） was constructed and validated.Results: We had screened out 9 necroptosis-related lncRNAs (BACE1-AS, LINC01188, LUCAT1, PI3KCD-AS2, Z83851.1, AC009283.1, AC012360.2, AC015908.3, AC103760.1), which were used to construct a predictive signature, and draw the receiver operating characteristic (ROC) curve by the high- and low-risk group. It was found that the area under the curve (AUC) of risk score was 0.874, and the AUCs values of 1-,3-,and 5-years were 0.8, 0.759, 0.787. The TCGA data were randomly divided into two cohorts. In two cohorts, The OS of the high-risk groups were significantly lower than that of the low-risk groups, and the AUC of the ROC curves of the two cohorts were 0.851, 0.804, 0.802 and 0.735, 0.716, 0.76 at 1-, 3-, and 5-years. After quantifying immune cell subsets and related functions, it was found that the infiltration of active dendritic cells (aDCs), macrophages, mast cells, natural killer cells (NK), T regulatory cells (Tregs) were significantly different, and the expressions of immune checkpoints CD86, LAIR1, CTLA4, VTCN1, TNFRSF18, CD80, CD276, HHLA2, TNFSF4, TNFRSF8, TNFRSF4, TNFRSF9, LGALS9, HAVCR2 and TNFSF15 were also significantly different.Conclusion: This predictive signature can accurately predict the prognosis of hepatocellular carcinoma patients and provide guidance for the clinical treatment of hepatocellular carcinoma patients.

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“…Their fine molecular regulation mechanisms have been widely revealed to be involved in cell apoptosis, proliferation and other biological processes. Studies have shown that lncRNAs play significant roles in the occurrence and evolution of diseases [ 6 , 7 ]. LncRNA CDKN2B-AS1, as a potential lncRNA, has been demonstrated to be abnormally expressed in various malignant tumors [ 8 ], including gastric cancer, lung cancer, and breast cancer, with implications in the proliferation and migration of tumor cells [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

CDKN2B antisense RNA 1 expression alleviates idiopathic pulmonary fibrosis by functioning as a competing endogenouse RNA through the miR-199a-5p/Sestrin-2 axis

Yang

Yin

et al. 2022

Bioengineered

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Idiopathic pulmonary fibrosis (IPF) is an idiopathic interstitial lung disease. At present, the pathogenesis of IPF has not been fully elucidated, which has affected the development of effective treatment methods. Here, we explored the function and potential mechanism of long noncoding RNA (lncRNA) CDKN2B antisense RNA 1 (CDKN2B-AS1) in IPF.Transforming growth factor-β (TGF-β) and bleomycin (BLM) were used to induce IPF in cells and animal models. Real Time quantitative Polymerase Chain Reaction (RT-qPCR) showed the expression of CDKN2B-AS1, miR-199a-5p and Sestrin-2 (SESN2) in cells and tissues. The double luciferase reporter gene assay confirmed the targeting relationship among CDKN2B-AS1, miR-199a-5p, and SESN2. Related protein levels were detected by Western blot combined with Cell Counting Kit-8 (CCK-8), wound healing, and flow cytometry to analyze cell proliferation, migration, and apoptosis. The pathological characteristics of mouse lung tissue were determined by Hematoxylin-eosin (HE) and Masson staining. We found that the expression of CDKN2B-AS1 was decreased in TGF-β-treated cells and BLM-treated mice. Overexpression of CDKN2B-AS1 inhibited cell proliferation and migration, promoted apoptosis, decreased the expression of fibrosis-related proteins and promoted autophagy. In addition, overexpression of CDKN2B-AS1 alleviated pulmonary fibrosis in BLM-treated mice. Mechanistically, CDKN2B-AS1 acts as a miR-199a-5p sponge to regulate SESN2 expression. Our results indicate the importance of the CDKN2B-AS1/miR-199a-5p/SESN2 axis.

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LncRNA AIRN influences the proliferation and apoptosis of hepatocellular carcinoma cells by regulating STAT1 ubiquitination

Cited by 30 publications

References 34 publications

LncRNA Airn alleviates diabetic cardiac fibrosis by inhibiting activation of cardiac fibroblasts via a m6A-IMP2-p53 axis

LncRNA Airn alleviates diabetic cardiac fibrosis by inhibiting activation of cardiac fibroblasts via a m6A-IMP2-p53 axis

Necroptosis-related lncRNAs and Hepatocellular Carcinoma Undoubtedly Secret

CDKN2B antisense RNA 1 expression alleviates idiopathic pulmonary fibrosis by functioning as a competing endogenouse RNA through the miR-199a-5p/Sestrin-2 axis

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