lncRNA ADAMTS9-AS2 Controls Human Mesenchymal Stem Cell Chondrogenic Differentiation and Functions as a ceRNA

Huang, Mingjian; Zhao, Jingyu; Xu, Jiajia; Li, Jing; Zhuang, Yifu; Zhang, Xiaoling

doi:10.1016/j.omtn.2019.08.027

Cited by 34 publications

(26 citation statements)

References 48 publications

(53 reference statements)

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“…Yang et al [17] confirm the tumor-promoting activity of miR-942-5p in NSCLC. The lncRNAs ADAMTS9-AS2 [18] and LINC00675 [14] have been reported to sponge miR-942-5p in mesenchymal stem cells and colorectal cancer cells, respectively. However, overexpression of either of the 2 lncRNAs did not affect the expression of miR-942-5p in NSCLC cells (data not shown).…”

Section: Introductionmentioning

confidence: 99%

lncRNA LIFR-AS1 suppresses invasion and metastasis of non-small cell lung cancer via the miR-942-5p/ZNF471 axis

Wang

Huang

et al. 2020

Cancer Cell Int

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Background: MicroRNA 942-5p (miR-942-5p) has been reported to promote migration and invasion in non-small cell lung cancer (NSCLC), but the underlying mechanism is not completely understood. The interplay between long noncoding RNAs (lncRNAs) and miRNAs plays a crucial role in tumor progression. Methods: In the present study, we performed bioinformatic and biochemical analyses to identify miR-942-5p-interacting lncRNAs. The function and clinical significance of the candidate lncRNA(s) in NSCLC were determined. Results: We identified LIFR-AS1 as a pivotal miR-942-5p-interacting lncRNA. Overexpression of miR-942-5p caused a reduction of LIFR-AS1 in NSCLC cells. LIFR-AS1 showed the ability to sponge miR-942-5p, leading to derepression of ZNF471. Functionally, LIFR-AS1 overexpression inhibited NSCLC cell migration and invasion, whereas LIFR-AS1 silencing yielded an opposite effect. In vivo studies confirmed that LIFR-AS1 overexpression suppressed lung metastasis of NSCLC cells. Rescue experiments demonstrated that enforced expression of miR-942-5p or depletion of ZNF471 restored the migration and invasion capacity of LIFR-AS1-overexpressing cells. Moreover, overexpression of ZNF471 restrained NSCLC cell invasion. Clinically, LIFR-AS1 downregulation was significantly correlated with TNM stage, lymph node metastasis, and reduced overall survival in NSCLC patients. Conclusions: we provide first evidence for the involvement of the LIFR-AS1/miR-942-5p/ZNF471 axis in NSCLC invasion and metastasis. LIFR-AS1 may represent a novel target for the treatment of NSCLC.

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Section: Introductionmentioning

confidence: 99%

lncRNA LIFR-AS1 suppresses invasion and metastasis of non-small cell lung cancer via the miR-942-5p/ZNF471 axis

Wang

Huang

et al. 2020

Cancer Cell Int

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“…In humans, ADAMTS9-AS2 was identified as an antisense transcript of the ADAMTS9 [ 51 ]. ADAMTS9-AS2 inhibits cell proliferation via the miR-27a-3p/FOXO1 axis in clear cell renal cell carcinoma [ 52 ] and controls the chondrogenic differentiation in human mesenchymal stem cells through a ceRNA mechanism [ 53 ]. In the present study, we originally speculated that Lnc-ADAMTS9 may function through ADAMTS9 in a lncRNA/mRNA pair manner.…”

Section: Discussionmentioning

confidence: 99%

Global transcriptomic analysis reveals Lnc-ADAMTS9 exerting an essential role in myogenesis through modulating the ERK signaling pathway

Wang

Zhang

et al. 2021

J Animal Sci Biotechnol

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Background Long non-coding RNAs (lncRNAs) are emerging key regulators involved in a variety of biological processes such as cell differentiation and development. The balance between myogenesis and adipogenesis is crucial for skeletal muscle homeostasis in humans and meat quality in farm animals. The present study aimed to reveal the global transcriptomic profiles of adipogenic (Adi-) and myogenic (Myo-) precursors derived from porcine skeletal muscle and identify lncRNAs involved in the modulation of myogenesis homeostasis in porcine skeletal muscle. Results In this study, a total of 655 novel individual lncRNAs including differentially expressed 24 lncRNAs, and 755 differentially expressed mRNAs were identified (fold change ≥2 or ≤ 0.5 and adjusted P < 0.05). Integrated results of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis accompanied by the variation of intracellular Ca2+ concentration highlighted Lnc-ADAMTS9 involved in the modulation of myogenesis homeostasis in porcine skeletal muscle. Although Lnc-ADAMTS9 knock-down did not alter the mRNA expression of ADAMTS9, we demonstrated that Lnc-ADAMTS9 can promote myogenic proliferation and myogenic differentiation of myogenic precursors through inhibiting the ERK/MAPK signaling pathway. Conclusion We deciphered a comprehensive catalog of mRNAs and lncRNAs that might be involved in the regulation of myogenesis and adipogenesis homeostasis in the skeletal muscle of pigs. The Lnc-ADAMTS9 exerts an essential role in myogenesis through the ERK signaling pathway.

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“…In a study to evaluate the chondrogenic differentiation of hMSCs, lncRNA ADAMTS9-AS2 has been reported to serve as a competing endogenous RNA for miR-942-5p, which is involved in regulating the expression of Scrg1, a transcription factor promoting chondrogenic gene expression. There, lncRNA ADAMTS9-AS2 controls hMSC chondrogenic differentiation ( Huang et al, 2019 ). We postulate that lnc-CYP7A1-1 may act in a similar fashion in competing with microRNAs to regulate SYNE1 and hBM-MSCs functions.…”

Section: Discussionmentioning

confidence: 99%

Down-Regulation of Lnc-CYP7A1-1 Rejuvenates Aged Human Mesenchymal Stem Cells to Improve Their Efficacy for Heart Repair Through SYNE1

Dong

Liu

Wen

et al. 2020

Front. Cell Dev. Biol.

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Background: Several long non-coding RNAs (lncRNAs) have been associated with cell senescence, termed senescence-associated lncRNAs (SAL-RNAs). However, the mechanisms involved for SAL-RNAs in aging are not fully elucidated. In the present study, we investigated the effects of SAL-RNAs on aged human bone marrow-derived mesenchymal stem cells (hBM-MSCs), and the possible means to counteract such effects to improve the regenerative capacity of aged hBM-MSCs. Methods: By comparing the lncRNAs expression of hBM-MSCs derived from young and old individuals, lnc-CYP7A1-1 was identified as being significantly increased with age. Using predictive software, the expression of Spectrin Repeat Containing Nuclear Envelope Protein 1 (SYNE1), was found to be decreased with age. Next, through lentiviral constructs, we downregulated the expression of lnc-CYP7A1-1 or SYNE1 in hBM-MSCs separately. Additionally, hBM-MSCs proliferation, survival, migration, and senescence were investigated in vitro. In vivo, lnc-CYP7A1-1 downregulated aged hBM-MSCs were implanted into infarcted mouse hearts after myocardial infarction (MI), and cardiac function was measured. Through lentivirus-mediated downregulation of lnc-CYP7A1-1 in aged hBM-MSCs, we revealed that cell senescence was decreased, whereas cell proliferation, migration, and survival were increased. On the other hand, downregulation of SYNE1, the target gene of lnc-CYP7A1-1, in young hBM-MSCs increased cell senescence, yet decreased cell proliferation, migration, and survival. Downregulation of lnc-CYP7A1-1 in aged hBM-MSCs induced cell rejuvenation, yet this effect was attenuated by repression of SYNE1. In vivo, transplantation of lnc-CYP7A1-1 downregulated old hBM-MSCs improved cardiac function after MI. Conclusion: Down-regulation of lnc-CYP7A1-1 rejuvenated aged hBM-MSCs and improved cardiac function when implanted into the infarcted mouse hearts, possibly through its target gene SYNE1.

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lncRNA ADAMTS9-AS2 Controls Human Mesenchymal Stem Cell Chondrogenic Differentiation and Functions as a ceRNA

Cited by 34 publications

References 48 publications

lncRNA LIFR-AS1 suppresses invasion and metastasis of non-small cell lung cancer via the miR-942-5p/ZNF471 axis

lncRNA LIFR-AS1 suppresses invasion and metastasis of non-small cell lung cancer via the miR-942-5p/ZNF471 axis

Global transcriptomic analysis reveals Lnc-ADAMTS9 exerting an essential role in myogenesis through modulating the ERK signaling pathway

Down-Regulation of Lnc-CYP7A1-1 Rejuvenates Aged Human Mesenchymal Stem Cells to Improve Their Efficacy for Heart Repair Through SYNE1

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