The role of miRNA, lncRNA and circRNA in the development of intervertebral disk degeneration (Review)

Jiang, Jian Fa; Sun, Yuxiu; Xu, Gaoran; Wang, Hong

doi:10.3892/etm.2021.9987

Cited by 15 publications

(15 citation statements)

References 88 publications

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“…The competing endogenous RNA (ceRNA) hypothesis is an important mechanism that allows circRNAs in cancers by sponging microRNAs (miRNAs) to modulate mRNAs [ 24 ]. Increasing evidence shows that the circRNA and miRNA can regulate apoptosis and autophagy of cells [ 7 , 25 , 26 ], including NP cells [ 27 ]. These identified ceRNA interaction aces may be crucial targets for treatment of IDD [ 28 ].…”

Section: Introductionmentioning

confidence: 99%

CircRNA RERE Promotes the Oxidative Stress-Induced Apoptosis and Autophagy of Nucleus Pulposus Cells through the miR-299-5p/Galectin-3 Axis

Wang¹,

Zhou

Luo³

et al. 2021

Journal of Healthcare Engineering

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Intervertebral disc degeneration (IDD) is widely accepted as a cause of low back pain and related degenerative musculoskeletal disorders. Nucleus pulposus (NP) cell loss is closely related to IDD progression. Thus, investigating the specifically targeted therapeutic agents against NP cell loss depends on understanding the molecular mechanisms. In this study, human NP cells were treated with hydrogen peroxide (H2O2). Cell viability was assessed by using the Cell Counting Kit-8 (CCK-8) kit. The expression of circRNA arginine-glutamic acid dipeptide repeats (hsa_circ_RERE) and miR-299-5p was analyzed by real-time quantitative PCR. Western blot analysis was used to assess the protein expression levels. The autophagy levels in NP cells were detected by using an electronic microscope, LC3B protein immunofluorescence, and western blot. The apoptosis levels of NP cells were detected by flow cytometry and western blot. Dual-luciferase reporter assay analyzed the miR-299-5p bound to circ_RERE and galectin-3. Our results revealed that H2O2 significantly inhibited the viability of NP cells, promoted apoptosis and autophagy, and upregulated galectin-3 expression. miR-299-5p was reduced in IDD and H2O2-induced NP cells. The overexpression of miR-299-5p promoted cell viability and attenuated apoptosis and autophagy under H2O2 treatment. Besides, circ_RERE was upregulated in IDD and H2O2-induced NP cells. However, knockdown of circ_RERE reversed the effects of miR-299-5p overexpression on cell viability, apoptosis, and autophagy in NP cells. We propose that circ_RERE promotes the H2O2-induced apoptosis and autophagy of NP cells through the miR-299-5p/galectin-3 axis and may provide a new target for the clinical treatment of IDD.

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Section: Introductionmentioning

confidence: 99%

CircRNA RERE Promotes the Oxidative Stress-Induced Apoptosis and Autophagy of Nucleus Pulposus Cells through the miR-299-5p/Galectin-3 Axis

Wang¹,

Zhou

Luo³

et al. 2021

Journal of Healthcare Engineering

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“…circRNAs act as competing endogenous RNAs to sponge miRNAs, and to subsequently regulate the expression of target genes ( 28 , 56 , 61 , 62 ). As Ma et al ( 8 ) reported, circ-UBAP2 knockdown inhibited the progression of OS cells by upregulating the expression of miR-204-3p and, thus, downregulating the expression of its target gene, HMGA2.…”

Section: Discussionmentioning

confidence: 99%

“…miR-141-3p functions as a tumor suppressor in OS, colorectal cancer and gastric cancer (24)(25)(26)(27). Additionally, in recent years, a number of studies have demonstrated that circRNAs can competitively bind to miRNAs, thereby eliminating the regulatory effect of miRNAs on their target genes and participating in tumor progression (28,29). For instance, in non-small cell lung carcinoma (NSCLC), circ_100395 inhibited NSCLC malignancy by sponging miR-141-3p and thereby increasing the expression levels of large tumor suppressor kinase 2 (30).…”

Section: Circ-lrp6 Contributes To Osteosarcoma Progression By Regulat...mentioning

confidence: 99%

circ‑LRP6 contributes to osteosarcoma progression by regulating the miR‑141‑3p/HDAC4/HMGB1 axis

Dong

Zheng

et al. 2022

Int J Oncol

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Circular RNA-lipoprotein receptor 6 (circ-LRP6) serves a role in promoting the tumorigenesis of retinoblastoma, esophageal squamous cell cancer and oral squamous cell carcinoma; however, whether circ-LRP6 demonstrates the same effect in osteosarcoma (OS) is yet to be fully elucidated.The present study aimed to analyze the expression, role and potential molecular mechanism of circ-LRP6 in OS. The expression levels of circ-LRP6, microRNA (miR)-141-3p, histone deacetylase 4 (HDAC4) and high mobility group protein 1 (HMGB1) were evaluated by reverse transcriptionquantitative PCR in OS tissues and cell lines. Cell Counting Kit-8, Transwell and Matrigel assays were conducted to evaluate cell proliferation, migration and invasion, respectively. Western blotting was also performed to determine HDAC4 and HMGB1 protein expression levels. Bioinformatics and dual-luciferase reporter assays were used to predict and analyze the interactions between circ-LRP6 and miR-141-3p, miR-141-3p and HDAC4, as well as between miR-141-3p and HMGB1. Additionally, RNA immunoprecipitation was performed to verify the association between circ-LRP6 and miR-141-3p. The results confirmed that circ-LRP6 was highly expressed in OS tissues and cell lines. In addition, circ-LRP6 negatively regulated the expression of miR-141-3p and, in turn, miR-141-3p negatively regulated HDAC4 and HMGB1 expression. Functional assays revealed that circ-LRP6 knockdown inhibited the proliferation, migration and invasion of OS cells, whereas the inhibition of miR-141-3p or the overexpression of either HDAC4 or HMGB1 partly reversed the inhibitory effect of circ-LRP6 knockdown. In summary, the present study determined that circ-LRP6 knockdown inhibited the proliferation, migration and invasion of OS cells by regulating the miR-141-3p/HDAC4/HMGB1 axis.

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“…The dysregulation of lncRNA expression influences apoptosis of disk cells, implying relevance in the development of intervertebral disk degeneration (IDD) 68,69 . OIP5‐AS1 has specifically been implicated in IDD where it has been found in a ceRNA network (along with KCNQ10T1 and UGDH‐AS1) to regulate hsa‐miR‐140, which is involved in cartilage development and osteoarthritis pathogenesis 70 .…”

Section: A Single Lncrna: a Myriad Diseasesmentioning

confidence: 99%

Long non‐coding RNA OIP5‐AS1 (Cyrano): A context‐specific regulator of normal and disease processes

Wooten

Smith

2022

Clinical & Translational Med

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Long non‐coding (lnc) RNAs have been implicated in a plethora of normal biological functions, and have also emerged as key molecules in various disease processes. OIP5‐AS1, also commonly known by the alias Cyrano, is a lncRNA that displays broad expression across multiple tissues, with significant enrichment in particular contexts including within the nervous system and skeletal muscle. Thus far, this multifaceted lncRNA has been found to have regulatory functions in normal cellular processes including cell proliferation and survival, as well as in the development and progression of a myriad disease states. These widespread effects on normal and disease states have been found to be mediated through context‐specific intermolecular interactions with dozens of miRNAs and proteins identified to date. This review explores recent studies to highlight OIP5‐AS1's contextual yet pleiotropic roles in normal homeostatic functions as well as disease oetiology and progression, which may influence its utility in the generation of future theranostics.

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The role of miRNA, lncRNA and circRNA in the development of intervertebral disk degeneration (Review)

Cited by 15 publications

References 88 publications

CircRNA RERE Promotes the Oxidative Stress-Induced Apoptosis and Autophagy of Nucleus Pulposus Cells through the miR-299-5p/Galectin-3 Axis

CircRNA RERE Promotes the Oxidative Stress-Induced Apoptosis and Autophagy of Nucleus Pulposus Cells through the miR-299-5p/Galectin-3 Axis

circ‑LRP6 contributes to osteosarcoma progression by regulating the miR‑141‑3p/HDAC4/HMGB1 axis

Long non‐coding RNA OIP5‐AS1 (Cyrano): A context‐specific regulator of normal and disease processes

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