The Combination of piR-823 and Eukaryotic Initiation Factor 3 B (EIF3B) Activates Hepatic Stellate Cells via Upregulating TGF-β1 in Liver Fibrogenesis

Tang, Xuechan; Xie, Xing; Wang, Xin; Wang, Yan; Jiang, Xiaoyu; Jiang, Hui‐Qing

doi:10.12659/msm.914222

Cited by 33 publications

(29 citation statements)

References 21 publications

(26 reference statements)

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“…In particular, EIF3B is a translation promoter of TGF-β1, which is a well-recognized factor in the pathogenesis of liver fibrosis; therefore, the interaction between piR-823 and EIF3B can induce a higher TGF-β1 expression that leads to greater activation of HSCs to initiate liver fibrosis. In this manner, piR-823 may be also considered a promising target in the treatment of liver fibrosis and, hence, its modulation would help to avoid the development of HCC [ 93 ].…”

Section: The Role Of Pirnas In Gastrointestinal (Gi) Cancersmentioning

confidence: 99%

The Emerging Role of PIWI-Interacting RNAs (piRNAs) in Gastrointestinal Cancers: An Updated Perspective

Riquelme

Pérez-Moreno

Letelier

et al. 2021

Cancers

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Gastrointestinal (GI) cancers produce ~3.4 million related deaths worldwide, comprising 35% of all cancer-related deaths. The high mortality among GI cancers is due to late diagnosis, the presence of metastasis and drug resistance development. Additionally, current clinical markers do not adequately guide patient management, thereby new and more reliable biomarkers and therapeutic targets are still needed for these diseases. RNA-seq technology has allowed the discovery of new types of RNA transcripts including PIWI-interacting RNAs (piRNAs), which have particular characteristics that enable these molecules to act via diverse molecular mechanisms for regulating gene expression. Cumulative evidence has described the potential role of piRNAs in the development of several tumor types as a likely explanation for certain genomic abnormalities and signaling pathways’ deregulations observed in cancer. In addition, these piRNAs might be also proposed as promising diagnostic or prognostic biomarkers or as potential therapeutic targets in malignancies. This review describes important topics about piRNAs including their molecular characteristics, biosynthesis processes, gene expression silencing mechanisms, and the manner in which these transcripts have been studied in samples and cell lines of GI cancers to elucidate their implications in these diseases. Moreover, this article discusses the potential clinical usefulness of piRNAs as biomarkers and therapeutic targets in GI cancers.

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Section: The Role Of Pirnas In Gastrointestinal (Gi) Cancersmentioning

confidence: 99%

The Emerging Role of PIWI-Interacting RNAs (piRNAs) in Gastrointestinal Cancers: An Updated Perspective

Riquelme

Pérez-Moreno

Letelier

et al. 2021

Cancers

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“…HSCs were isolated from male C57 mice according to previously reports [26]. Briefly, the mice were euthanised by cervical dislocation after anesthetizing with a mixture of Ketamine (75 mg/kg) and Medetomidine (1 mg/kg), and then the liver was perfused by portal vein using Pronase-E (Sigma-Aldrich) and collagenase (A005275, Sangon Biotech, Shanghai, China).…”

Section: Primary Hscs Isolation and Cell Culturementioning

confidence: 99%

Saikosaponin-d alleviates hepatic fibrosis through regulating GPER1/autophagy signaling

et al. 2021

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Background Hepatic fibrosis is the final pathway of chronic liver disease characterized by excessive accumulation of extracellular matrix (ECM), which eventually develop into cirrhosis and liver cancer. Emerging studies demonstrated that Saikosaponin-d (SSd) exhibits a protective role in liver fibrosis. However, the mechanism underlying anti-liver fibrosis of SSd in vivo and in vitro remains unclear. Methods and results Transforming growth factor (TGF)-β and carbon tetrachloride (CCl4) were used for creating liver fibrosis model in vitro and in vivo, respectively. The role of SSd in regulating liver fibrosis was assessed through Sirius red and Masson staining, and IHC assay. We found that SSd attenuated remarkably CCl4-induced liver fibrosis as evidenced by decreased collagen level, and decreased expression of fibrotic markers Col 1 and α-SMA. Meanwhile, SSd repressed autophagy activation as suggested by decreased BECN1 expression and increased p62 expression. Compared with HSCs from CCl4-treated group, the primary HSCs from SSd-treated mice exhibited a marked inactivation of autophagy. Mechanistically, SSd treatment enhanced the expression of GPER1 in primary HSCs and in TGF-β-treated LX-2 cells. GPER1 agonist G1 repressed autophagy activation, whereas GPER1 antagonist G15 activated autophagy and G15 also damaged the function of SSd on suppressing autophagy, leading to subsequent increased levels of fibrotic marker level in LX-2 cells. Conclusions Our findings highlight that SSd alleviates hepatic fibrosis by regulating GPER1/autophagy pathway.

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“…74 Furthermore, piR-823 promoted the production of a-smooth muscle actin (a-SMA), and collagen type I alpha 1 (COL1a), as well as components of extracellular matrix, which finally resulted in cirrhosis. 75 piR-Hep1 may have a role in suppressing cell death by activating the signal transducer and activator of transcription 3 (Stat3)/Bcl-x L signaling pathway. 76 Actually, most HCCs develop from cirrhosis for which hepatitis B virus infection and alcohol abuse are the most common causes.…”

Section: Liver Cancermentioning

confidence: 99%

The Biogenesis and Functions of piRNAs in Human Diseases

Pan

Fang

et al. 2020

Molecular Therapy - Nucleic Acids

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Piwi-interacting RNAs (piRNAs) are a novel type of small noncoding RNAs, which are 26-30 nt in length and bind to Piwi proteins. These short RNAs were originally discovered in germline cells and are considered as key regulators for germline maintenance. A growing body of evidence has now extended our views into piRNA biological significance showing that they can also regulate gene expression in somatic cells through transposon silencing, epigenetic programming, DNA rearrangements, mRNA turnover, and translational control. Mounting studies have revealed that the dysregulation of piRNAs may cause epigenetic changes and contribute to diverse diseases. This review illustrates piRNA biogenesis, mechanisms behind piRNA-mediated gene regulation, and changes of piRNAs in different diseases, especially in cancers. Biogenesis of piRNAs Generation of PrecursorsA large proportion of piRNA precursors are produced from genetic regions named piRNA clusters, which can be divided into uni-strand or dual-strand clusters. Uni-strand clusters give rise to precursors mapping only to one strand, whereas dual-strand clusters produce precursors mapping to both genomic strands. Additionally, some piRNA precursors can be generated from the 3 0 UTR of protein-coding genes, or from individual transposons. 21,22 The transcription of uni-strand clusters is similar to the canonical mRNA transcription. Uni-strand clusters harbor the transcriptionassociated histone 3 lysine 4 demethylation (H3K4me2) mark at promoters. Additionally, piRNA precursors are 5 0 methyl-guanosine capped and 3 0 terminated. 23,24 On the contrary, dual-strand clusters lack clear signatures of RNA polymerase II (RNA Pol II) promoters, such

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The Combination of piR-823 and Eukaryotic Initiation Factor 3 B (EIF3B) Activates Hepatic Stellate Cells via Upregulating TGF-β1 in Liver Fibrogenesis

Cited by 33 publications

References 21 publications

The Emerging Role of PIWI-Interacting RNAs (piRNAs) in Gastrointestinal Cancers: An Updated Perspective

The Emerging Role of PIWI-Interacting RNAs (piRNAs) in Gastrointestinal Cancers: An Updated Perspective

Saikosaponin-d alleviates hepatic fibrosis through regulating GPER1/autophagy signaling

The Biogenesis and Functions of piRNAs in Human Diseases

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