LncRNA-miRNA axis in tumor progression and therapy response: An emphasis on molecular interactions and therapeutic interventions

Entezari, Maliheh; Taheriazam, Afshin; Orouei, Sima; Fallah, Shayan; Sanaei, Arezoo; Hejazi, Elahe Sadat; Kakavand, Amirabbas; Rezaei, Shamin; Heidari, Hajar; Behroozaghdam, Mitra; Daneshi, Salman; Salimimoghadam, Shokooh; Mirzaei, Sepideh; Hashemi, Mehrdad; Samarghandian, Saeed

doi:10.1016/j.biopha.2022.113609

Cited by 42 publications

(23 citation statements)

References 245 publications

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“…On the other hand, overexpression of miR-9-5 p can also lead to NEAT1 decrease. It is shown that miRNAs can modulate the expression level of lncRNAs in an Argonaute2 (Ago2)-dependent manner, and lncRNAs mainly decrease miRNA expression via sponging [53,54]. These could be the possible mechanisms of how NEAT1 and miR-9-5 p can regulate each other.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 regulates HCV-induced Hepatocellular carcinoma by modulating the miR-9-BGH3 axis

Tripathi

Pal

Ghosh

et al. 2022

Journal of General Virology

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Chronic hepatitis C virus (HCV) infection is a leading cause of end-stage liver diseases, such as fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Several cellular entities, including paraspeckles and their related components, are involved in viral pathogenesis and cancer progression. NEAT1 lncRNA is a major component of paraspeckles that has been linked to several malignancies. In this study, analysis of the Cancer Genome Atlas (TCGA) database and validation in HCV-induced HCC tissue and serum samples showed significantly high expression of NEAT1 in patients with liver cancer. Moreover, we found that NEAT1 levels increased upon HCV infection. To further understand the mechanism of NEAT1-induced HCC progression, we selected one of its targets, miR-9–5 p, which regulates BGH3 mRNA levels. Interestingly, miR-9–5 p levels were downregulated upon HCV infection, whereas BGH3 levels were upregulated. Additionally, partial NEAT1 knockdown increased miR-9–5 p levels and decreased BGH3 levels, corroborating our initial results. BGH3 levels were also upregulated in HCV-induced HCC and TCGA tissue samples, which could be directly correlated with NEAT1 levels. As a known oncogene, BGH3 is directly linked to HCC progression mediated by NEAT1. We also found that NEAT1 levels remained upregulated in serum samples from patients treated with direct-acting antivirals (DAA), indicating that NEAT1 might be a molecular trigger that promotes HCC development. Collectively, these findings provide molecular insights into HCV-induced HCC progression via the NEAT1-miR-9-BGH3 axis.

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Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 regulates HCV-induced Hepatocellular carcinoma by modulating the miR-9-BGH3 axis

Tripathi

Pal

Ghosh

et al. 2022

Journal of General Virology

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“…These effects have been best studied in cancer where lncRNA‐miRNA axes regulate apoptosis and autophagy. Moreover, these axes influence tumour metastases through regulation of epithelial‐mesenchymal transition (EMT) and expression of matrix metalloproteinase 5 …”

Section: Introductionmentioning

confidence: 99%

“…Moreover, these axes influence tumour metastases through regulation of epithelial-mesenchymal transition (EMT) and expression of matrix metalloproteinase. 5 MIR100HG, alternatively named as Mir-100-Let-7a-2-Mir-125b-1 Cluster Host Gene, is encoded by a gene located on chr11:122,028,203-122,556,721 (Figure 1). The gene encoding this lncRNA has 17 exons.…”

Section: Introductionmentioning

confidence: 99%

A concise review on the role of MIR100HG in human disorders

Ghafouri‐Fard

Harsij

Farahzadi

et al. 2023

J Cellular Molecular Medi

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MIR100HG is a long non‐coding RNA (lncRNA) encoded by a locus on chr11:122,028,203‐122,556,721. This gene can regulate cell proliferation, apoptosis, cell cycle transition and cell differentiation. MIR100HG was firstly identified through a transcriptome analysis and found to regulate differentiation of human neural stem cells. It is functionally related with a number of signalling pathways such as TGF‐β, Wnt, Hippo and ERK/MAPK signalling pathways. Dysregulation of MIR100HG has been detected in a diversity of cancers in association with clinical outcomes. Moreover, it has a role in the pathophysiology of dilated cardiomyopathy, intervertebral disk degeneration and pulmonary fibrosis. The current study summarizes the role of these lncRNAs in human disorders.

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“…Overexpression of LINC00152 has been shown to promote the expression of fascin actin-binding protein 1 (FSCN1) by binding mir-632 and mir-185-3p, leading to proliferation and metastasis [19]. As reviewed in 2022, lncRNAs including DCST1-AS1, LINC01569, KCNQ1OT1, and LINC00997 were considered to take an active part in carcinogenesis by infuencing cell metastasis, drug resistance, radio-resistance, and tumor microenvironment interaction [20]. However, the role of lncRNAs in COAD has not been completely elucidated.…”

Section: Introductionmentioning

confidence: 99%

A Prognostic Cuproptosis-Related LncRNA Signature for Colon Adenocarcinoma

Zhong

Zhu

Shen

et al. 2023

Journal of Oncology

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Background. Cuproptosis, a recently discovered form of cell death, is caused by copper levels exceeding homeostasis thresholds. Although Cu has a potential role in colon adenocarcinoma (COAD), its role in the development of COAD remains unclear. Methods. In this study, 426 patients with COAD were extracted from the Cancer Genome Atlas (TCGA) database. The Pearson correlation algorithm was used to identify cuproptosis-related lncRNAs. Using the univariate Cox regression analysis, the least absolute shrinkage and selection operator (LASSO) was used to select cuproptosis-related lncRNAs associated with COAD overall survival (OS). A risk model was established based on the multivariate Cox regression analysis. A nomogram model was used to evaluate the prognostic signature based on the risk model. Finally, mutational burden and sensitivity analyses of chemotherapy drugs were performed for COAD patients in the low- and high-risk groups. Result. Ten cuproptosis-related lncRNAs were identified and a novel risk model was constructed. A signature based on ten cuproptosis-related lncRNAs was an independent prognostic predictor for COAD. Mutational burden analysis suggested that patients with high-risk scores had higher mutation frequency and shorter survival. Conclusion. Constructing a risk model based on the ten cuproptosis-related lncRNAs could accurately predict the prognosis of COAD patients, providing a fresh perspective for future research on COAD.

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LncRNA-miRNA axis in tumor progression and therapy response: An emphasis on molecular interactions and therapeutic interventions

Cited by 42 publications

References 245 publications

LncRNA NEAT1 regulates HCV-induced Hepatocellular carcinoma by modulating the miR-9-BGH3 axis

LncRNA NEAT1 regulates HCV-induced Hepatocellular carcinoma by modulating the miR-9-BGH3 axis

A concise review on the role of MIR100HG in human disorders

A Prognostic Cuproptosis-Related LncRNA Signature for Colon Adenocarcinoma

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