Recent advances of long noncoding RNAs involved in the development of multiple sclerosis

Li, Qianwen; Lei, Wen; Chen, Cong; Guo, Wei

doi:10.1016/s1875-5364(20)30003-0

Cited by 7 publications

(10 citation statements)

References 103 publications

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“…Likewise, He et al study about nonsmall lung cancer added that MAGI2-AS3 attenuates the proliferation and progression of the disease through the miRNA-23a-3p/PTEN pathway . Ample evidence has reported the deep role of lncRNAs and miRNAs in mediating inflammatory and immunological diseases through targeting major transcription factors and vital intracellular signaling pathways . Indeed, the current research is the first documentation of the interconnection among MAGI2-AS3/miR-374b-5p and PTEN in MS patients.…”

Section: Discussionmentioning

confidence: 72%

“…Early evidence has revealed that the interaction between lncRNAs and miRNAs acts as influential and potential modifiers in MS. − Noncoding RNAs have been shown to be involved in diverse processes in the pathogenesis of MS, including immune system regulation and chronic inflammatory responses. , MAGI2 antisense RNA 3 (MAGI2-AS3) (gene ID: 100505881; ensemble; ENSG00000234456) is a novel type of lncRNA comprising 18252 bp, 8 exons and located on chromosome 7q21.11. Databases revealed that MAGI2-AS3 is widely expressed in fats, ovaries, and other tissues and is interrelated with cell proliferation, metastasis, and treatment resistance in several types of cancer. , Furthermore, the association between MAGI2-AS3 and chronic inflammatory diseases, neurotoxicity, and neuro-inflammation has also been reported .…”

Section: Introductionmentioning

confidence: 99%

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MAGI2-AS3 and miR-374b-5p as Putative Regulators of Multiple Sclerosis via Modulating the PTEN/AKT/IRF-3/IFN-β Axis: New Clinical Insights

Kortam

Elfar

Shaker

et al. 2023

ACS Chem. Neurosci.

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Multiple sclerosis (MS) is a chronic disease and one of the leading causes of disability in young adults. The current study aims to investigate the pathogenesis of MS via studying the regulatory role of novel lncRNA MAGI2-AS3 in miR-374b-5p and their downstream targets PTEN/AKT/IRF-3/IFN-β and the relationship of this pathway with disease severity. Moreover, it aims to assess the role of MAGI2-AS3/miR-374b-5p as diagnostic and/or prognostic biomarkers for MS. Overall, 150 contributors were recruited: 100 patients with MS and 50 healthy volunteers. Gene expression of MAGI2-AS3, miR-374b-5p, PTEN, AKT, and IRF-3 were assessed using RT-qPCR, and IFN-β was measured by ELISA. Compared with the healthy control group, serum MAGI2-AS3 and PTEN were downregulated in MS patients, whereas miR-374b-5p, PI3K, AKT, IRF-3, and IFN-β were upregulated in MS patients. Furthermore, MAGI2-AS3 was downregulated, while miR-374b-5p was upregulated in MS patients with an expanded disability status scale (EDSS) ≥3.5, compared to patients with an EDSS <3.5. Receiver-operating-characteristic curve analysis revealed that MAGI2-AS3 and miR-374b-5p can be used in the diagnosis of MS. Remarkably, multivariate logistic analysis revealed that MAGI2-AS3, miR-374b-5p, PTEN, and AKT act as independent variables in MS. Moreover, MAGI2-AS3 was directly correlated with PTEN and inversely correlated with miR-374b-5p, AKT, and EDSS. Regarding miR-374b-5p, it was positively correlated with AKT and EDSS. In conclusion, the study showed for the first time that the crosstalk between MAGI2-AS3 and miR-374b-5p could affect the AKT/IRF3/IFN-β axis in MS. Interestingly, MAGI2-AS3 and miR-374b-5p could be genetic noninvasive biomarkers for MS.

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Section: Discussionmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

MAGI2-AS3 and miR-374b-5p as Putative Regulators of Multiple Sclerosis via Modulating the PTEN/AKT/IRF-3/IFN-β Axis: New Clinical Insights

Kortam

Elfar

Shaker

et al. 2023

ACS Chem. Neurosci.

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“…Large amount of evidence has revealed the regulatory mechanisms of lncRNA on functional proteins. 56 , 57 , 58 Our previous studies have reported that lncRNAs, such as lncR‐ZFAS1, lncR‐CCRR and lnR‐MIAT, could inhibit the protein function through directly binding to its functional region. 13 , 16 , 17 Consistent with the previous studies, here we found that lncR‐SMAL reduced Parkin protein levels both in whole cell lysate and mitochondrial content and restricted the mito‐translocation of Parkin.…”

Section: Discussionmentioning

confidence: 99%

“…Large amount of evidence has revealed the regulatory mechanisms of lncRNA on functional proteins 56–58 . Our previous studies have reported that lncRNAs, such as lncR‐ZFAS1, lncR‐CCRR and lnR‐MIAT, could inhibit the protein function through directly binding to its functional region 13,16,17 .…”

Section: Discussionmentioning

confidence: 99%

LncRNA LOC105378097 inhibits cardiac mitophagy in natural ageing mice

Liu

Bai

Liu

et al. 2022

Clinical & Translational Med

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1) The heart-enriched lncR-SMAL is robustly increased in its level in serum samples of human subjects over 60-year old relative to young controls, and in both nucleus and cytoplasm of senescent cardiomyocytes. (2) Artificial overexpression of lncR-SMAL induces cardiac senescence by inhibiting Parkinmediated mitophagy. Knockdown of endogenous lncR-SMAL in cardiomyocytes partially abrogated cell senescence. (3) LncR-SMAL interacts with Parkin protein and promotes ubiquitin-proteasome degradation of Parkin in senescent cardiomyocytes.

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“…Instead of regulating TYMS, H19 may sponge miR-194-5p to trigger the autophagy process via the SIRT1 enzyme [ 308 ]. Effective inhibition of these lncRNAs can be achieved through small interfering RNAs (siRNAs), RNA destabilizing elements (RDEs), antisense oligonucleotides (ASOs), and ribozymes; all of which had been demonstrated to target lncRNAs with high specificity [ 309 , 310 ]. In fact, recently, patisiran represents the world’s first siRNA-based drug that is FDA-approved for the treatment of hereditary transthyretin-mediated amyloidosis via transthyretin (TTR) gene silencing [ 311 ].…”

Section: Reversal Strategiesmentioning

confidence: 99%

Recent Updates on Mechanisms of Resistance to 5-Fluorouracil and Reversal Strategies in Colon Cancer Treatment

Azwar

Seow

Abdullah

et al. 2021

Biology

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5-Fluorouracil (5-FU) plus leucovorin (LV) remain as the mainstay standard adjuvant chemotherapy treatment for early stage colon cancer, and the preferred first-line option for metastatic colon cancer patients in combination with oxaliplatin in FOLFOX, or irinotecan in FOLFIRI regimens. Despite treatment success to a certain extent, the incidence of chemotherapy failure attributed to chemotherapy resistance is still reported in many patients. This resistance, which can be defined by tumor tolerance against chemotherapy, either intrinsic or acquired, is primarily driven by the dysregulation of various components in distinct pathways. In recent years, it has been established that the incidence of 5-FU resistance, akin to multidrug resistance, can be attributed to the alterations in drug transport, evasion of apoptosis, changes in the cell cycle and DNA-damage repair machinery, regulation of autophagy, epithelial-to-mesenchymal transition, cancer stem cell involvement, tumor microenvironment interactions, miRNA dysregulations, epigenetic alterations, as well as redox imbalances. Certain resistance mechanisms that are 5-FU-specific have also been ascertained to include the upregulation of thymidylate synthase, dihydropyrimidine dehydrogenase, methylenetetrahydrofolate reductase, and the downregulation of thymidine phosphorylase. Indeed, the successful modulation of these mechanisms have been the game plan of numerous studies that had employed small molecule inhibitors, plant-based small molecules, and non-coding RNA regulators to effectively reverse 5-FU resistance in colon cancer cells. It is hoped that these studies would provide fundamental knowledge to further our understanding prior developing novel drugs in the near future that would synergistically work with 5-FU to potentiate its antitumor effects and improve the patient’s overall survival.

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Recent advances of long noncoding RNAs involved in the development of multiple sclerosis

Cited by 7 publications

References 103 publications

MAGI2-AS3 and miR-374b-5p as Putative Regulators of Multiple Sclerosis via Modulating the PTEN/AKT/IRF-3/IFN-β Axis: New Clinical Insights

MAGI2-AS3 and miR-374b-5p as Putative Regulators of Multiple Sclerosis via Modulating the PTEN/AKT/IRF-3/IFN-β Axis: New Clinical Insights

LncRNA LOC105378097 inhibits cardiac mitophagy in natural ageing mice

Recent Updates on Mechanisms of Resistance to 5-Fluorouracil and Reversal Strategies in Colon Cancer Treatment

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