lncRNA in the liver: Prospects for fundamental research and therapy by RNA interference

Smekalova, Elena M.; Kotelevtsev, Yuri; Leboeuf, Dominique; Shcherbinina, Evgeniya; Fefilova, Anna S.; Zatsepin, Timofei S.; Koteliansky, Victor

doi:10.1016/j.biochi.2016.06.007

Cited by 34 publications

(26 citation statements)

References 167 publications

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“… 4 , 5 In HCC, lncRNAs have been demonstrated to participate in cell proliferation, migration and invasion. 6 , 7 For example, lncRNA-AWPPH has been reported to promote cell proliferation and migration in HCC. 8 Shen et al have indicated that lncRNA TATDN1 accelerates proliferation and cell cycle progression in HCC.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: LncRNA RHPN1-AS1 Promotes Cell Proliferation, Migration and Invasion Through Targeting miR-7-5p and Activating PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

Song

Ren

et al. 2020

Technol Cancer Res Treat

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Hepatocellular carcinoma (HCC) is a severe disease with high mortality in the world. Emerging evidence has suggested that lncRNAs play an important role in cancer progression, including HCC. This study aimed to comprehensively investigate the effect of lncRNA RHPN1 antisense RNA 1 (RHPN1-AS1) on HCC and its underlying molecular mechanism. In this study, we evaluated the expressions of lncRNA RHPN1-AS1 and miR-7-5p by qRT-RCR in both HCC tissue and HCC cells. Our findings showed that lncRNA RHPN1-AS1 was upregulated in HCC tissue and HCC cells, while miR-7-5p was downregulated. LncRNA RHPN1-AS1 expression in HCC patients was closely related to vascular invasion, tumor-node-metastasis (TNM) stage and barcelona clinic liver cancer (BCLC) stage. Furthermore, we quantified cell clone-formation ability, proliferation, migration and invasion of HCCLM3 and MHCC97 H cells using several assays (colony formation assay, 5-Ethynyl-2′-deoxyuridine (EdU) assay and transwell assay, respectively). Functional experiments confirmed that silencing lncRNA RHPN1-AS1 inhibited cell proliferation, migration and invasion in HCCLM3 and MHCC97 H cells. After that, bioinformatics analysis, dual luciferase reporter gene assay, qRT-PCR and western blot were used to investigate the molecular mechanism of lncRNA RHPN1-AS1 on HCC. Mechanistically, the rescue experiments demonstrated that miR-7-5p inhibitor reversed the inhibition effect of silencing lncRNA RHPN1-AS1 on HCCLM3 cells proliferation, migration and invasion. Moreover, silencing lncRNA RHPN1-AS1 also inhibited the activation of PI3K/AKT/mTOR pathway. Taken together our findings demonstrated that lncRNA RHPN1-AS1 could facilitate cell proliferation, migration and invasion via targeting miR-7-5p and activating PI3K/AKT/mTOR pathway in HCC.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: LncRNA RHPN1-AS1 Promotes Cell Proliferation, Migration and Invasion Through Targeting miR-7-5p and Activating PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

Song

Ren

et al. 2020

Technol Cancer Res Treat

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“…Therefore, the suppression of activated HSCs is important for preventing liver fibrosis . Many lncRNAs have been found involved in the activation of HSCs and liver fibrosis . In this study, we demonstrated for the first time that XIST expression was upregulated in ethanol‐activated HSCs (LX‐2) and livers from ALF model rats.…”

Section: Discussionmentioning

confidence: 69%

“…Long noncoding RNAs (lncRNAs) represent a specific class of ncRNA molecules with transcript lengths >200 nucleotides. Many lncRNAs have been reported to be involved in the HSCs activation and liver fibrosis . For example, lncRNA HOX transcript antisense RNA (HOTAIR) facilitates HSCs activation and fibrogenesis in the mouse livers .…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA XIST enhances ethanol‐induced hepatic stellate cells autophagy and activation via miR‐29b/HMGB1 axis

et al. 2019

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Activation of hepatic stellate cells (HSCs) is a prominent driver of liver fibrogenesis, including alcoholic liver fibrosis (ALF). Furthermore, autophagy contributes to HSCs activation. This study aims to investigate the role and the mechanisms of long noncoding RNA XIST in regulating HSCs autophagy and activation. Human HSC cells (LX-2) were treated with 100 mmol/L ethanol to mimic HSCs activation. The HSCs activation was evaluated by determining cell viability and protein levels of fibrosis markers α-smooth muscle actin (α-SMA) and collagen type 1 α1 (CoL1A1). The autophagy was evaluated by measuring autophagy markers Beclin-1 and LC3-II. The interaction among XIST, miR-29b, and high-mobility group box-1 (HMGB1) were analyzed using luciferase reporter assay, qRT-PCR, and western blot. Lentiviruses targeting sh-XIST (LV-sh-XIST) were injected into ALF model mice via tail vein to elucidate the in vivo role of XIST in ALF injury. XIST was upregulated in ethanolactivated LX-2 cells. Furthermore, XIST served as a competitive endogenous RNA of miR-29b to facilitate HMGB1 expression, and thus enhanced ethanol-induced HSCs autophagy and activation. Further in vivo assay showed that downregulation of XIST by LV-sh-XIST alleviated ALF injury in ALF model mice. Collectively, XIST enhances ethanol-induced HSCs autophagy and activation via miR-29b/HMGB1 axis.autophagy, hepatic stellate cells activation, HMGB1, miR-29b, XIST Abbreviations: ALF, alcoholic liver fibrosis; CoL1A1, collagen type 1 α1; ceRNA, competitive endogenous RNA; HMGB, high mobility group protein B1; HMGB1, high-mobility group box-1; HSCs, hepatic stellate cells; HOTAIR, lncRNA HOX transcript antisense RNA; lncRNAs, long noncoding RNAs; LC3-II, microtubule-associated protein 1A/1B-light chain 3; LV-sh-XIST, lentiviruses targeting sh-XIST; LX-2, human HSC cells; MTT, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide; PF, pulmonary fibrosis; RNA XIST, long noncoding; si-HMGB1, small interfering RNA targeting HMGB1; siRNA, small interfering RNA; si-XIST, small interfering RNA targeting XIST; XIST, LncRNA X-inactive-specific transcript; α-SMA, α-smooth muscle actin.

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“…In addition to the physiologic impact of lncRNAs in metabolic organs, their dysregulation is also implicated in metabolic diseases. Thus, modulation of lncRNA expression holds a promising potential for therapeutic applications [ 120 ], and due to the fact that lncRNAs can also circulate via exosomes—maybe as part of the inter-organ crosstalk—they also provide the opportunity to be used as biomarkers for diagnostic applications [ 121 ].…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNAs in Metabolic Organs and Energy Homeostasis

Giroud

Scheideler

2017

IJMS

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Single cell organisms can surprisingly exceed the number of human protein-coding genes, which are thus not at the origin of the complexity of an organism. In contrast, the relative amount of non-protein-coding sequences increases consistently with organismal complexity. Moreover, the mammalian transcriptome predominantly comprises non-(protein)-coding RNAs (ncRNA), of which the long ncRNAs (lncRNAs) constitute the most abundant part. lncRNAs are highly species- and tissue-specific with very versatile modes of action in accordance with their binding to a large spectrum of molecules and their diverse localization. lncRNAs are transcriptional regulators adding an additional regulatory layer in biological processes and pathophysiological conditions. Here, we review lncRNAs affecting metabolic organs with a focus on the liver, pancreas, skeletal muscle, cardiac muscle, brain, and adipose organ. In addition, we will discuss the impact of lncRNAs on metabolic diseases such as obesity and diabetes. In contrast to the substantial number of lncRNA loci in the human genome, the functionally characterized lncRNAs are just the tip of the iceberg. So far, our knowledge concerning lncRNAs in energy homeostasis is still in its infancy, meaning that the rest of the iceberg is a treasure chest yet to be discovered.

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lncRNA in the liver: Prospects for fundamental research and therapy by RNA interference

Cited by 34 publications

References 167 publications

RETRACTED: LncRNA RHPN1-AS1 Promotes Cell Proliferation, Migration and Invasion Through Targeting miR-7-5p and Activating PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

RETRACTED: LncRNA RHPN1-AS1 Promotes Cell Proliferation, Migration and Invasion Through Targeting miR-7-5p and Activating PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

Long noncoding RNA XIST enhances ethanol‐induced hepatic stellate cells autophagy and activation via miR‐29b/HMGB1 axis

Long Non-Coding RNAs in Metabolic Organs and Energy Homeostasis

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