LincRNA-p21 Inhibits the Wnt/β-Catenin Pathway in Activated Hepatic Stellate Cells via Sponging MicroRNA-17-5p

Yu, Fang; Guo, Yong; Chen, Bicheng; Shi, Liang; Dong, Peihong; Zhou, Mengtao; Zheng, Jianjian

doi:10.1159/000472410

Cited by 48 publications

(40 citation statements)

References 38 publications

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“…Hepatic stellate cells (HSCs), the primary effector cells in the liver, are involved in the development of pathological fibrosis [23, 24]. Thus, insight into mechanisms that regulate HSC activation is considered key for the treatment of hepatic fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Trolline Ameliorates Liver Fibrosis by Inhibiting the NF-κB Pathway, Promoting HSC Apoptosis and Suppressing Autophagy

Bai¹,

Huang²,

Nie³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Previous studies have shown that trolline possesses various forms of pharmacological activity, including antibacterial and antiviral potency. The present paper addressed the putative hepatoprotective effects of trolline. Methods: Rats received 2 ml/kg CCl₄ (mixed 1: 1 in peanut oil) intragastrically twice a week for 8 weeks to induce hepatic fibrosis. The animals were then treated with trolline for additional 4 weeks. Liver pathology and collagen accumulation were observed by hematoxylin-eosin and Masson’s trichrome staining, respectively. Serum transaminase activity and collagen-related indicator level were determined by commercially available kits. NF-κB pathway activation was also examined. Moreover, the effects of trolline on hepatic stellate cell (HSC-T6) apoptosis, mitochondrial membrane potential (MMP), and autophagy were assessed. Results: Trolline significantly alleviated CCl₄-induced liver injury and notably reduced the accumulation of collagen in liver tissues. Trolline treatment also markedly decreased inflammatory cytokines levels by inhibiting the NF-κB pathway. Trolline strongly inhibited HSC-T6 activation and notably induced cell apoptosis by modulating the Bax/Bcl-2 ratio, caspase activity, and MMP. Moreover, trolline significantly inhibited HSC-T6 autophagy, as evidenced by the decrease in the formation of autophagic vacuoles and the number of autophagosomes, by regulating the expression levles of LC3, Beclin-1, P62, Atg 5 and 7. Conclusion: Our study demonstrates that trolline ameliorates liver fibrosis, possibly by inhibiting the NF-κB pathway, promoting HSCs apoptosis and suppressing autophagy.

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Section: Discussionmentioning

confidence: 99%

Trolline Ameliorates Liver Fibrosis by Inhibiting the NF-κB Pathway, Promoting HSC Apoptosis and Suppressing Autophagy

Bai¹,

Huang²,

Nie³

et al. 2017

Cell Physiol Biochem

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“…[15][16][17] Increasing studies suggested that lncRNAs played crucial roles in the initiation and development of tumor and deregulated expression of lncRNAs was found in several tumors. [27][28][29] Previous studies showed that lincRNA-p21 suppressed the hepatocellular carcinoma and colorectal cancer progression. [22][23][24][25][26] LincR-NA-p21 is a novel lncRNA, which was identified as one direct transcriptional target gene of p53.…”

Section: Introductionmentioning

confidence: 99%

LincRNA‐p21 enhances the sensitivity of radiotherapy for gastric cancer by targeting the β‐catenin signaling pathway

Chen

Yuan

Yang

et al. 2018

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNAs) are a large and diverse class of transcribed RNA molecules with a length of more than 200 nucleotides that modulate the gene expression at the posttranscriptional or transcriptional level. LncRNAs played crucial roles in many biological processes, such as cell proliferation, metastasis, and migraton. In this study, we evaluated the role of lincRNA‐p21 in the gastric cancer (GC). We demonstrated that the expression level of lincRNA‐p21 was downregulated in the GC tissues and cell lines. Moreover, ectopic expression of lincRNA‐p21 suppressed the GC cell growth, cell cycle, and migration. Furthermore, we demonstrated that the X‐ray increased the expression level of lincRNA‐p21 in both the HCG‐27 and SGC7901 cells and elevated expression of lincRNA‐p21 increased the radiotherapy sensitivity of the GC cell. In addition, we showed that ectopic expression of lincRNA‐p21 suppressed the β‐catenin and c‐myc expression. Overexpression of lincRNA‐p21 inhibited the GC cell proliferation and increased the radiosensitivity of GC cells by regulating the β‐catenin signaling pathway. These data suggested that lincRNA‐p21 acted as a tumor suppressor gene in the development of GC.

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“…lincRNA‐p21 enhanced PTEN expression by competitively binding to miR‐181b (Yu, Lu, Chen, Dong, & Zheng, ). Yu, Guo, et al () reported that lincRNA‐p21, a target of miR‐17‐5p, inhibits miR‐17‐5p level. Lack of the miR‐17‐5p binding site in lincRNA‐p21 prevented the inhibition of miR‐17‐5p expression.…”

Section: Dysregulation Of Lncrnas In Liver Fibrosismentioning

confidence: 99%

“…lincRNA-p21 enhanced PTEN expression by competitively binding to miR-181b (Yu, Lu, Chen, Dong, & Zheng, 2016). Yu, Guo, et al (2017) Knockdown of lncRNA-ATB could downregulate β-catenin expression by upregulating the endogenous miR-200a and suppress the activation of LX-2 cells. Yu, Zheng, Mao, Dong, Lu, Li, et al (2015) reported that GAS5 is downregulated in liver fibrosis and in activated HSCs, whereas GAS5 overexpression inhibits the activation of HSCs.…”

Section: The Interaction Of Lncrnas With Mirnasmentioning

confidence: 99%

New advances of lncRNAs in liver fibrosis, with specific focus on lncRNA–miRNA interactions

Bian

Xiong

2018

Journal Cellular Physiology

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Noncoding RNAs (ncRNAs) were initially thought to be transcriptional byproducts. However, recent advances of ncRNAs research have increased our understanding of the importance of ncRNA in gene regulation and disease pathogenesis. Consistent with these developments, liver fibrosis research is also experiencing rapid growth in the investigation of links between ncRNAs and the pathology of this disease. The initial focus was on studying the function and regulation mechanisms of microRNAs (miRNAs). However, recently, elucidation of the mechanisms of long noncoding RNAs (lncRNAs) and lncRNA-mediated liver fibrosis has just commenced. In this review, we emphasize on abnormal expression of lncRNAs in liver fibrosis. Furthermore, we also discuss that the interaction of lncRNAs with miRNAs is involved in the regulation of the expression of protein-coding genes in liver fibrosis. Recent advances in understanding dysregulated lncRNAs expression and the lncRNAs-miRNAs interaction in liver fibrosis will help for developing new therapeutic targets and biomarkers of liver fibrosis.

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LincRNA-p21 Inhibits the Wnt/β-Catenin Pathway in Activated Hepatic Stellate Cells via Sponging MicroRNA-17-5p

Cited by 48 publications

References 38 publications

Trolline Ameliorates Liver Fibrosis by Inhibiting the NF-κB Pathway, Promoting HSC Apoptosis and Suppressing Autophagy

Trolline Ameliorates Liver Fibrosis by Inhibiting the NF-κB Pathway, Promoting HSC Apoptosis and Suppressing Autophagy

LincRNA‐p21 enhances the sensitivity of radiotherapy for gastric cancer by targeting the β‐catenin signaling pathway

New advances of lncRNAs in liver fibrosis, with specific focus on lncRNA–miRNA interactions

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