Role of Long Non-Coding RNAs in Conferring Resistance in Tumors of the Nervous System

Ghafouri‐Fard, Soudeh; Agabalazadeh, Amin; Abak, Atefe; Shoorei, Hamed; Taheri, Mohammad; Sharifi, Guive

doi:10.3389/fonc.2021.670917

Cited by 13 publications

(10 citation statements)

References 64 publications

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“…Furthermore, prior reviews have also primarily concentrated on common lncRNAs noted to have chemoresistance roles without extensive exploration of chemosensitivity of specific lncRNAs. 14 In contrast, this review aims to frame the TMZ response in GBM via exploration of the lncRNAs mediating the three major mechanisms of TMZ resistance: (1) regulation of the DDR, (2) maintenance of glioma stem cell (GSC) identity, and (3) exploitation of hypoxia-associated responses ( Table 1 ).…”

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confidence: 99%

Modulating glioblastoma chemotherapy response: Evaluating long non-coding RNA effects on DNA damage response, glioma stem cell function, and hypoxic processes

Yuan

Liu

Lee

et al. 2022

Neuro-Oncology Advances

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Glioblastoma (GBM) is the most common and aggressive primary adult brain tumor, with an estimated annual incidence of 17,000 new cases in the United States. Current treatments for GBM include chemotherapy, surgical resection, radiation therapy, and antiangiogenic therapy. However, despite the various therapeutic options, the five-year survival rate remains at a dismal 5%. Temozolomide (TMZ) is the first line chemotherapy drug for GBM; however, poor TMZ response is one of the main contributors to the dismal prognosis. Long non-coding RNAs (lncRNAs) are non-protein coding transcripts greater than 200 nucleotides that have been implicated to mediate various GBM pathologies, including chemoresistance. In this review, we aim to frame the TMZ response in GBM via exploration of the lncRNAs mediating three major mechanisms of TMZ resistance: 1) regulation of the DNA damage response, 2) maintenance of glioma stem cell identity, and 3) exploitation of hypoxia-associated responses.

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confidence: 99%

Modulating glioblastoma chemotherapy response: Evaluating long non-coding RNA effects on DNA damage response, glioma stem cell function, and hypoxic processes

Yuan

Liu

Lee

et al. 2022

Neuro-Oncology Advances

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“…NORAD, mainly induced by DNA damage, was initially identified as a lncRNA that played crucial roles in DNA protection and chromosomal stability [35]. Recent studies have demonstrated that NORAD acts as an oncogene in multiple cancers including malignant melanoma, pancreatic cancer, NSCLC and glioblastoma [36][37][38][39]. Importantly, NORAD has been reported to be correlated with chemotherapy resistance in cancer cells, such as resistance to doxorubicin, CDDP and oxaliplatin in neuroblastoma, NSCLC and gastric cancer, respectively [40][41][42].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA NORAD/miR-224-3p/MTDH axis contributes to CDDP resistance of esophageal squamous cell carcinoma by promoting nuclear accumulation of β-catenin

et al. 2021

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Background Cis-diamminedichloro-platinum (CDDP)-based chemotherapy regimens are the most predominant treatment strategies for patients with esophageal squamous cell carcinoma (ESCC). Dysregulated long non-coding RNAs (lncRNAs) contribute to CDDP resistance, which results in treatment failure in ESCC patients. However, the majority of lncRNAs involved in CDDP resistance in ESCC remain to be elucidated. Methods The public Gene Expression Omnibus (GEO) dataset GSE45670 was analysed to reveal potential lncRNAs involved in CDDP resistance of ESCC. Candidate upregulated lncRNAs were detected in ESCC specimens by qRT-PCR to identify crucial lncRNAs. Non-coding RNA activated by DNA damage (NORAD) was selected for further study. Kaplan-Meier analysis and a COX proportional regression model were performed to analyse the potential of NORAD for predicting prognosis of ESCC patients. The role of NORAD in CDDP resistance were determined by conducting gain and loss-of-function experiments in vitro. Fluorescence in situ hybridization (FISH) was performed to determine the subcellular location of NORAD in ESCC cells. A public GEO dataset and bioinformatic algorithms were used to predict the microRNAs (miRNAs) that might be latently sponged by NORAD. qRT-PCR was conducted to verify the expression of candidate miRNAs. Luciferase reporter and Argonaute-2 (Ago2)-RNA immunoprecipitation (RIP) assays were conducted to evaluate the interaction between NORAD and candidate miRNAs. A miRNA rescue experiment was performed to authenticate the NORAD regulatory axis and its effects on CDDP resistance in ESCC cells. Western blotting was conducted to confirm the precise downstream signalling pathway of NORAD. A xenograft mouse model was established to reveal the effect of NORAD on CDDP resistance in vivo. Results The expression of NORAD was higher in CDDP-resistant ESCC tissues and cells than in CDDP-sensitive tissues and cells. NORAD expression was negatively correlated with the postoperative prognosis of ESCC patients who underwent CDDP-based chemotherapy. NORAD knockdown partially arrested CDDP resistance of ESCC cells. FISH showed that NORAD was located in the cytoplasm in ESCC cells. Furthermore, overlapping results from bioinformatic algorithms analyses and qRT-PCR showed that NORAD could sponge miR-224-3p in ESCC cells. Ago2-RIP demonstrated that NORAD and miR-224-3p occupied the same Ago2 to form an RNA-induced silencing complex (RISC) and subsequently regulated the expression of metadherin (MTDH) in ESCC cells. The NORAD/miR-224-3p/MTDH axis promoted CDDP resistance and progression in ESCC cells by promoting nuclear accumulation of β-catenin in vitro and in vivo. Conclusions NORAD upregulates MTDH to promote CDDP resistance and progression in ESCC by sponging miR-224-3p. Our results highlight the potential of NORAD as a therapeutic target in ESCC patients receiving CDDP-based chemotherapy.

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“…Expression of non-coding RNAs might also affect response to therapeutic regimens [ 76 ]. For instance, H19 increases ATG7 expression and influences resistance to dopamine agonists [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

The Emerging Role of Non-Coding RNAs in Pituitary Gland Tumors and Meningioma

Ghafouri‐Fard

Abak

Hussen

et al. 2021

Cancers

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Long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs) are non-coding transcripts which are involved in the pathogenesis of pituitary gland tumors. LncRNAs that participate in the pathogenesis of pituitary gland tumors mainly serve as sponges for miRNAs. CLRN1-AS1/miR-217, XIST/miR-424-5p, H19/miR-93a, LINC00473/miR-502-3p, SNHG7/miR-449a, MEG8/miR-454-3p, MEG3/miR-23b-3p, MEG3/miR-376B-3P, SNHG6/miR-944, PCAT6/miR-139-3p, lncRNA-m433s1/miR-433, TUG1/miR-187-3p, SNHG1/miR-187-3p, SNHG1/miR-302, SNHG1/miR-372, SNHG1/miR-373, and SNHG1/miR-520 are identified lncRNA/miRNA pairs that are involved in this process. Hsa_circ_0001368 and circOMA1 are two examples of circRNAs that contribute to the pathogenesis of pituitary gland tumors. Meanwhile, SNHG1, LINC00702, LINC00460, and MEG3 have been found to partake in the pathogenesis of meningioma. In the current review, we describe the role of non-coding RNAs in two types of brain tumors, i.e., pituitary tumors and meningioma.

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Role of Long Non-Coding RNAs in Conferring Resistance in Tumors of the Nervous System

Cited by 13 publications

References 64 publications

Modulating glioblastoma chemotherapy response: Evaluating long non-coding RNA effects on DNA damage response, glioma stem cell function, and hypoxic processes

Modulating glioblastoma chemotherapy response: Evaluating long non-coding RNA effects on DNA damage response, glioma stem cell function, and hypoxic processes

Long non-coding RNA NORAD/miR-224-3p/MTDH axis contributes to CDDP resistance of esophageal squamous cell carcinoma by promoting nuclear accumulation of β-catenin

The Emerging Role of Non-Coding RNAs in Pituitary Gland Tumors and Meningioma

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