scholarly journals The Triangle Relationship Between Long Noncoding RNA, RIG-I-like Receptor Signaling Pathway, and Glycolysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhihua Ren ◽  
Yueru Yu ◽  
Chaoxi Chen ◽  
Dingyong Yang ◽  
Ting Ding ◽  
...  
Keyword(s):  
Viral Replication ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Aerobic Glycolysis ◽  
Lactate Production ◽  
Antiviral Immunity ◽  
Antiviral Immune Response ◽  
Downstream Signaling ◽  
New Perspective ◽  
Mitochondrial Antiviral Signaling

Long noncoding RNA (LncRNA), a noncoding RNA over 200nt in length, can regulate glycolysis through metabolic pathways, glucose metabolizing enzymes, and epigenetic reprogramming. Upon viral infection, increased aerobic glycolysis providzes material and energy for viral replication. Mitochondrial antiviral signaling protein (MAVS) is the only protein-specified downstream of retinoic acid-inducible gene I (RIG-I) that bridges the gap between antiviral immunity and glycolysis. MAVS binding to RIG-I inhibits MAVS binding to Hexokinase (HK2), thereby impairing glycolysis, while excess lactate production inhibits MAVS and the downstream antiviral immune response, facilitating viral replication. LncRNAs can also regulate antiviral innate immunity by interacting with RIG-I and downstream signaling pathways and by regulating the expression of interferons and interferon-stimulated genes (ISGs). Altogether, we summarize the relationship between glycolysis, antiviral immunity, and lncRNAs and propose that lncRNAs interact with glycolysis and antiviral pathways, providing a new perspective for the future treatment against virus infection, including SARS-CoV-2.

scholarly journals Long noncoding RNA PCA3 regulates glycolysis, viability and apoptosis by mediating the miR-1/CDK4 axis in prostate cancer

RSC Advances ◽  
2018 ◽  
Vol 8 (66) ◽  
pp. 37564-37572 ◽  
Author(s):  
Shuo Gu ◽  
Xiaobing Niu ◽  
Fei Mao ◽  
Zongyuan Xu
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Aerobic Glycolysis ◽  
Prostate Cancer Cells

We proved that PCA3 regulated aerobic glycolysis, viability and apoptosis by regulating the miR-1/CDK4 axis in prostate cancer cells.

scholarly journals Long noncoding RNA KCNQ1OT1 promotes colorectal carcinogenesis by enhancing aerobic glycolysis via hexokinase-2

Aging ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 11685-11697
Author(s):  
Cheng Chen ◽  
Meng Wei ◽  
Chao Wang ◽  
Danping Sun ◽  
Peng Liu ◽  
...  
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Aerobic Glycolysis ◽  
Colorectal Carcinogenesis ◽  
Hexokinase 2

scholarly journals Long noncoding RNA LINC01391 restrained gastric cancer aerobic glycolysis and tumorigenesis via targeting miR-12116/CMTM2 axis

2020 ◽  
Vol 11 (21) ◽  
pp. 6264-6276
Author(s):  
Cuijuan Qian ◽  
Zhurong Xu ◽  
Luyan Chen ◽  
Yichao Wang ◽  
Jun Yao
Keyword(s):  
Gastric Cancer ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Aerobic Glycolysis

scholarly journals Peroxisomes as Platforms for Cytomegalovirus’ Evasion from Cellular Antiviral Signaling

Proceedings ◽  
2020 ◽  
Vol 50 (1) ◽  
pp. 43
Author(s):  
Ana Rita Ferreira ◽  
Ana Gouveia ◽  
Mariana Marques ◽  
Daniela Ribeiro
Keyword(s):  
Immune Response ◽  
Mitochondrial Fission ◽  
Signaling Cascade ◽  
Peroxisomal Membrane ◽  
Antiviral Signaling ◽  
Antiviral Immune Response ◽  
Viral Propagation ◽  
Downstream Signaling ◽  
Dependent Inhibition ◽  
Mitochondrial Antiviral Signaling

Peroxisomes, in concert with mitochondria, have been established as platforms for the establishment of a rapid and stable antiviral immune response, due to the presence of the mitochondrial antiviral signaling protein (MAVS) at their membranes. Upon intracellular recognition of viral RNA, retinoic acid inducible gene-I (RIG-I)-like proteins interact with MAVS, inducing its oligomerization and the establishment of a signaling cascade that culminates with the production of direct antiviral effectors, preventing important steps in viral propagation. We and others have demonstrated that different viruses have developed specific mechanisms to counteract peroxisome-dependent antiviral signaling. We have shown that the human cytomegalovirus (HCMV) protein vMIA hijacks the peroxisome transport machinery to travel to the organelle, interact with MAVS, and inhibit the immune response. Here, we further unravel the mechanisms by which HCMV is able to evade peroxisome-dependent antiviral signaling. We demonstrate that vMIA localizes at the peroxisomes in a complex with MAVS and the stimulator of interferon genes (STING) protein. Furthermore, vMia interacts with mitochondrial fission factor (MFF) at the peroxisomal membrane, which we show to be essential for vMia-dependent inhibition of the antiviral immune response. Importantly, we demonstrate that vMIA’s interaction with MAVS impedes its oligomerization and the consequent activation of the downstream signaling cascade. Interestingly, our results underline important differences between vMIA’s mechanisms of action at the peroxisomes and the mitochondria. Our results unravel novel mechanisms involving the interplay between the HCMV and peroxisomes that may ultimately contribute to the discovery of novel targets for antiviral combat.

scholarly journals Long noncoding RNA DLEU2 drives the malignant behaviors of thyroid cancer through mediating the miR-205-5p/TNFAIP8 axis

2021 ◽  
Vol 10 (4) ◽  
pp. 471-483
Author(s):  
Jiwen Yang ◽  
Yayin Huang ◽  
Bohan Dong ◽  
Yunhai Dai
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Aerobic Glycolysis ◽  
Xenograft Model ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Thyroid Cancer Cells

Objective Considering the plight in thyroid cancer therapy, we aimed to find novel therapeutic targets from a molecular perspective. Methods Quantitative real-time PCR (qRT-PCR) and Western blot assay were carried out to determine RNA and protein expression. Cell counting kit-8 (CCK8) assay, flow cytometry, transwell migration assay and aerobic glycolysis analysis were performed to analyze cell proliferation, apoptosis, migration and aerobic glycolysis of thyroid cancer cells. MiRcode and Starbase software were used to search the downstream genes of long noncoding RNA (lncRNA) deleted in lymphocytic leukemia 2 (DLEU2) and microRNA-205-5p (miR-205-5p), and the intermolecular combination was confirmed by dual-luciferase reporter assay. The in vivo role of DLEU2 in tumor growth was verified using the murine xenograft model. Results DLEU2 and tumor necrosis factor-α-induced protein 8 (TNFAIP8) were highly expressed in thyroid cancer tissues and cell lines. DLEU2 and TNRAIP8 promoted the proliferation, migration and aerobic glycolysis and restrained the apoptosis of thyroid cancer cells. DLEU2/miR-205-5p/TNFAIP8 signaling axis was identified in thyroid cancer cells. TNFAIP8 overexpression largely rescued the malignant phenotypes in DLEU2-silenced thyroid cancer cells. DLEU2 positively regulated TNFAIP8 expression by acting as miR-205-5p sponge in thyroid cancer cells. DLEU2 silencing blocked the growth of xenograft tumors in vivo. Conclusion lncRNA DLEU2 exerted a pro-tumor role to promote proliferation, migration and aerobic glycolysis while repressing the apoptosis of thyroid cancer cells via miR-205-5p/TNFAIP8 axis.

scholarly journals Long Noncoding RNA MIR210HG Promotes the Warburg Effect and Tumor Growth by Enhancing HIF-1α Translation in Triple-Negative Breast Cancer

2020 ◽  
Vol 10 ◽  
Author(s):  
Ye Du ◽  
Na Wei ◽  
Ruolin Ma ◽  
Shu-Heng Jiang ◽  
Dong Song
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Long Noncoding Rna ◽  
Warburg Effect ◽  
Noncoding Rna ◽  
Triple Negative ◽  
Lactate Production ◽  
Luciferase Reporter ◽  
Loss Of Function ◽  
The Warburg Effect

BackgroundHypoxia is an important environmental factor and has been correlated with tumor progression, treatment resistance and poor prognosis in many solid tumors, including triple-negative breast cancer (TNBC). Emerging evidence suggests that long noncoding RNA (lncRNA) functions as a critical regulator in tumor biology. However, little is known about the link between hypoxia and lncRNAs in TNBC.MethodsTNBC molecular profiles from The Cancer Genome Atlas (TCGA) were leveraged to identify hypoxia-related molecular alterations. Loss-of-function studies were performed to determine the regulatory role of MIR210HG in tumor glycolysis. The potential functions and mechanisms of hypoxia-MIR210HG axis were explored using qPCR, Western blotting, luciferase reporter assay, and polysome profiling.ResultsWe found that MIR210HG is a hypoxia-induced lncRNA in TNBC. Loss-of-function studies revealed that MIR210HG promoted the Warburg effect as demonstrated by glucose uptake, lactate production and expression of glycolytic components. Mechanistically, MIR210HG potentiated the metabolic transcription factor hypoxia-inducible factor 1α (HIF-1α) translation via directly binding to the 5’-UTR of HIF-1α mRNA, leading to increased HIF-1a protein level, thereby upregulating expression of glycolytic enzymes. MIR210HG knockdown in TNBC cells reduced their glycolytic metabolism and abolished their tumorigenic potential, indicating the glycolysis-dependent oncogenic activity of MIR210HG in TNBC. Moreover, MIR210HG was highly expressed in breast cancer and predicted poor clinical outcome.ConclusionOur results decipher a positive feedback loop between hypoxia and MIR210HG that drive the Warburg effect and suggest that MIR210HG may be a good prognostic marker and therapeutic target for TNBC patients.

scholarly journals Long noncoding RNA SLC2A1‐AS1 regulates aerobic glycolysis and progression in hepatocellular carcinoma via inhibiting the STAT3/FOXM1/GLUT1 pathway

2020 ◽  
Vol 14 (6) ◽  
pp. 1381-1396 ◽  
Author(s):  
Runze Shang ◽  
Miao Wang ◽  
Bin Dai ◽  
Jianbing Du ◽  
Jianlin Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Aerobic Glycolysis

scholarly journals Long Noncoding RNA GAS6-AS1 Inhibits Progression and Glucose Metabolism Reprogramming in Lung Adenocarcinoma Via Repressing E2F1-Mediated Transcription of GLUT1

2020 ◽  
Author(s):  
Jing Luo ◽  
Huishan Wang ◽  
Li Wang ◽  
Gaoming Wang ◽  
Yu Yao ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Lung Adenocarcinoma ◽  
Cancer Progression ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Ectopic Expression ◽  
Lactate Production ◽  
Luciferase Reporter

Abstract BackgroundGlucose metabolism reprogramming is one of the hallmarks of cancer cells. While functional and regulatory mechanism of long noncoding RNA (lncRNA) in the contribution of glucose metabolism in lung adenocarcinoma (LUAD) remains incompletely understood. The aim of this study was to uncover the roles for GAS6-AS1 in the regulation of progression and glucose metabolism in LUAD.MethodsThe tumor-suppressive function of GAS6-AS1 was determined by experiments in vitro and nude mice xenograft models. The role of GAS6-AS1 in regulating cancer glucose metabolism was proved by detecting glucose uptake, lactate production, pyruvate production and extracellular acidification rate (ECAR). RNA pull-down assay, RNA immunoprecipitation (RIP) assay, luciferase reporter assay and Chromatin Immunoprecipitation (ChIP) assay were used to identify the underlying molecular mechanisms of GAS6-AS1. And the expression level of GAS6-AS1 in LUAD tissues and cells was measured by quantitative real-time PCR.ResultsOverexpression of GAS6-AS1 suppressed tumor progression of LUAD both in vitro and in vivo. Metabolic-related assays revealed that GAS6-AS1 inhibited glucose metabolism reprogramming. Mechanically, GAS6-AS1 was found to repress the expression of glucose transporter GLUT1, a key regulator of glucose metabolism. Ectopic expression of GLUT1 restored the inhibition effect of GAS6-AS1 on cancer progression and glucose metabolism reprogramming. Further investigation identified that GAS6-AS1 directly interacted with transcription factor E2F1 and suppressed E2F1-mediated transcription of GLUT1. And GAS6-AS1 was downregulated in LUAD tissues and correlated with clinicopathological characteristics and survival of patients.ConclusionsTaken together, our results identified GAS6-AS1 as a novel tumor suppressor in LUAD and unraveled its underlying molecular mechanism in reprogramming glucose metabolism. GAS6-AS1 potentially served as a prognostic marker and therapeutic target in LUAD.

Sign in / Sign up

Export Citation Format

Share Document