Role of miRNA and lncRNAs in organ fibrosis and aging

Ghafouri‐Fard, Soudeh; Abak, Atefe; Talebi, Seyedeh Fahimeh; Shoorei, Hamed; Branicki, Wojciech; Taheri, Mohammad; Dilmaghani, Nader Akbari

doi:10.1016/j.biopha.2021.112132

Cited by 82 publications

(25 citation statements)

References 144 publications

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“…Long noncoding RNAs (lncRNAs) are a type of RNA, generally defined as transcripts more than 200 nucleotides that are not translated into protein. It has been thought that proteins carry genetic information for a long time, but more and more evidence has demonstrated that lncRNAs are also involved in regulated gene expression and affect growth and development of organisms [ 18 ]. Compared with short-chain RNAs, lncRNAs may play more complex biological function.…”

Section: Introductionmentioning

confidence: 99%

lncRNA AGAP2-AS1 Facilitates Tumorigenesis and Ferroptosis Resistance through SLC7A11 by IGF2BP2 Pathway in Melanoma

Huang

et al. 2022

Computational and Mathematical Methods in Medicine

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Long noncoding RNAs (lncRNAs) stand as indispensable regulators of initiation and development in melanoma (melanoma). However, the action molecular mechanisms linked to melanoma remain unclear. In the current study, the findings revealed that AGAP2-AS1 was considerably greater in melanoma than in healthy tissues and that the level of AGAP2-AS1 in cancer tissue was significantly linked to the cancerous TNM stage of patients. Individuals with high AGAP2-AS1 had a considerably shorter survival duration than patients with low AGAP2-AS1, regardless of progression-free survival or overall survival. Functionally, downregulating the expression of AGAP2-AS1 can inhibit the growth of melanocytes. Compared with the control group, AGAP2-AS1 knockdown increased Erastin-mediated iron death in melanoma cells. However, iron death inhibitor FERSINT-1 restored this effect, while Erastin induced melanoma cell death. Besides, intracellular iron and Fe2+ levels increased after AGAP2-AS1 knockdown in melanoma cells treated with Erastin compared with the si-NC group. In addition, AGAP2-AS1 silencing resulted in a significant decrease in glutathione (GSH) content in Erastin-treated melanoma cells. The mechanistic results suggest AGAP2-AS1 increases SLC7A11 mRNA stability through the IGF2BP2 pathway. In this investigation, we discovered new activities for AGAP2-AS1 and firstly discovered its mechanistic basis in ferroptosis and melanoma formation that might help in the search for potential therapy options in melanoma.

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Section: Introductionmentioning

confidence: 99%

lncRNA AGAP2-AS1 Facilitates Tumorigenesis and Ferroptosis Resistance through SLC7A11 by IGF2BP2 Pathway in Melanoma

Huang

et al. 2022

Computational and Mathematical Methods in Medicine

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“…Studies have demonstrated that lncRNAs are essential in the pathogenesis of fibrosis [ 8 ] and tumorigenesis [ 7 ]. However, studies of lncRNAs in the occurrence and malignant progression of OSF are still in nascent.…”

Section: Discussionmentioning

confidence: 99%

Low LINC02147 expression promotes the malignant progression of oral submucous fibrosis

Liu

Xie

2022

BMC Oral Health

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Background Key lncRNAs associated with the malignant progression of oral submucous fibrosis (OSF) to oral squamous cell carcinoma (OSCC) were identified. Methods Key lncRNAs with sequential changes from normal oral mucosa (NOM) to OSF to OSCC were identified based on the GEO database. Kaplan–Meier analysis was used to screen lncRNAs related to OSCC prognosis. Cox regression analysis was used to validate the independent prognostic value. qPCR was used to confirm the expression of the candidate lncRNAs. Gene set enrichment analysis (GSEA), nucleocytoplasmic separation assay, fluorescence in situ hybridization, RNA knockdown, western blot, and cell viability assay were performed to investigate the biological functions of the candidate lncRNA. A nomogram was constructed to quantitatively predict OSCC prognosis based on TCGA. Results Bioinformatics methods indicated that LINC02147 was sequentially downregulated from NOM to OSF to OSCC, as confirmed by clinical tissues and cells. Meanwhile, low LINC02147 expression, as an independent prognostic factor, predicted a poor prognosis for OSCC. GSEA and in vitro studies suggested that low LINC02147 expression promoted OSF malignant progression by promoting cell proliferation and differentiation. A LINC02147 signature-based nomogram successfully quantified each indicator’s contribution to the overall survival of OSCC. Conclusions Low LINC02147 expression promoted OSF malignant progression and predicted poor OSCC prognosis.

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“…and circRNAs [6][7][8][9]. circRNA is a novel type of non-coding RNA characterized by a covalent closed-loop structure without 5' to 3' ends or a poly-A tail.…”

Section: Introductionmentioning

confidence: 99%

Suppressing circ_0008494 inhibits HSC s activation by regulating the miR-185-3p/ Col1a1 axis

Li¹,

Zhou²,

Luo

et al. 2022

Preprint

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Background Because of its viral nature and the increasingly metabolic chronic liver diseases, hepatic fibrosis (HF) has become a major challenge to global health. However, there are still no approved effective therapies for HF. Circular RNAs (circRNAs) have emerged as new potential targets of liver diseases. Thus, this research aims to clarify the role of circ_0008494 in liver fibrosis and reveal its mechanism. Methods circRNA profiles were screened by RNA sequencing and the location of circ_0008494 was confirmed by fluorescence in situ hybridization assay in human liver fibrosis tissues. Bioinformatics analysis was used for result prediction and dual luciferase reporter, together with AGO-RIP and biotin-coupled miRNA capture assays, were used to determine miR-185-3p/collagen type I alpha 1 chain (Col1a1) as the target of circ_0008494. A stable circ_0008494-interfering cell line of the hepatic stellate cells (HSCs) was constructed and used to determine the regulatory mechanism of circ_0008494/ miR-185-3p/ Col1a1 axis. Results Hsa_circ_0008494 was significantly over-expressed and uniquely located at the cytoplasm of HSCs in human HF tissues. Together, dual luciferase reporter, AGO-RIP and biotin-coupled miRNA capture assays validated that circ_0008494 acted as a sponge of miR-185-3p. Rescue assays demonstrated suppressing circ_0008494 could inhibit HSCs’ activation, proliferation, migration and promote their apoptosis through miR-185-3p. In particular, the fibrosis indicator, Col1a1, was predicted as the direct target of miR-185-3p and the suppression of circ_0008494 inhibited the expression of Col1a1 by releasing miR-185-3p. Conclusions Knocking down circ_0008494 ameliorated fibrosis through the miR-185-3p/Col1a1 axis. circ_0008494 could be a promising treatment target for hepatic fibrosis.

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Role of miRNA and lncRNAs in organ fibrosis and aging

Cited by 82 publications

References 144 publications

lncRNA AGAP2-AS1 Facilitates Tumorigenesis and Ferroptosis Resistance through SLC7A11 by IGF2BP2 Pathway in Melanoma

lncRNA AGAP2-AS1 Facilitates Tumorigenesis and Ferroptosis Resistance through SLC7A11 by IGF2BP2 Pathway in Melanoma

Low LINC02147 expression promotes the malignant progression of oral submucous fibrosis

Suppressing circ_0008494 inhibits HSC s activation by regulating the miR-185-3p/ Col1a1 axis

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