LncRNA NEAT1 Knockdown Inhibits Retinoblastoma Progression by miR-3619-5p/LASP1 Axis

Chen, Xuedong; Zhao, Shiyong; Liu, Qingjun; Xu, Caicai; Yu, Yongbin; Ge, Heng

doi:10.3389/fgene.2020.574145

Cited by 12 publications

(6 citation statements)

References 24 publications

(12 reference statements)

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“…The contribution of NEAT1 to cancer progression has also been studied in other cancers, including cervical cancer [ 77 ], cholangiocarcinoma [ 78 ], endometrial cancer [ 79 ], esophageal carcinoma [ 80 ], gallbladder cancer [ 81 ], glioblastoma [ 82 ], Hodgkin’s lymphoma [ 83 ], laryngeal carcinoma [ 84 ], melanoma [ 85 ], multiple myeloma [ 11 ], nasopharyngeal carcinoma [ 86 ], osteosarcoma [ 87 ], pancreatic carcinoma [ 88 ], retinoblastoma [ 89 ], thyroid cancer [ 90 ], and tongue carcinoma [ 91 ]. In those cancers, NEAT1 plays a pro-proliferative role and promotes the progression of cancer by upregulating the expression of some oncogenes or downregulating the expression of some tumor suppressor genes.…”

Section: Neat1 Sponges Micrornas and Stabilizes Mrnasmentioning

confidence: 99%

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Zhang

et al. 2022

Cancers

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As one of the best-studied long noncoding RNAs, nuclear paraspeckle assembly transcript 1 (NEAT1) plays a pivotal role in the progression of cancers. NEAT1, especially its isoform NEAT1-1, facilitates the growth and metastasis of various cancers, excluding acute promyelocytic leukemia. NEAT1 can be elevated via transcriptional activation or stability alteration in cancers changing the aggressive phenotype of cancer cells. NEAT1 can also be secreted from other cells and be delivered to cancer cells through exosomes. Hence, elucidating the molecular interaction of NEAT1 may shed light on the future treatment of cancer. Herein, we review the molecular function of NEAT1 in cancer progression, and explain how NEAT1 interacts with RNAs, proteins, and DNA promoter regions to upregulate tumorigenic factors.

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Section: Neat1 Sponges Micrornas and Stabilizes Mrnasmentioning

confidence: 99%

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Zhang

et al. 2022

Cancers

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“…Bioinformatics analyses in the present study were able to confirm the association between the upregulation of LASP1 expression in liver cancer and liver cancer prognosis. Further studies have reported that LASP1 is involved in cellular migration, invasion, proliferation and apoptosis through several mechanisms, such as participation in signaling pathways, m6A methylation modification or influencing the tumor microenvironment (30)(31)(32)(33)(34). In addition, progress has been made in terms of ongoing therapeutic research seeking to target LASP1 (35).…”

Section: Discussionmentioning

confidence: 99%

lncRNA PAARH impacts liver cancer cell proliferation by engaging miR‑6512‑3p to target LASP1

Wei,

Liu,

Huang

et al. 2024

Oncol Lett

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Long non-coding (lnc)RNAs serve a pivotal role as regulatory factors in carcinogenesis. The present study aimed to assess the involvement of the lncRNA progression and angiogenesis-associated RNA in hepatocellular carcinoma (PAARH) in liver cancer, along with the associated underlying mechanism. Through the use of reverse transcription-quantitative (RT-q)PCR, differences in the expression levels of PAARH in HepG2, HEP3B2.1.7, HCCLM3, Huh-7 and MHCC97-H liver cancer cell lines and THLE-2 epithelial cell lines were evaluated. The liver cancer cell line with the greatest, significantly different, level of expression relative to the normal liver cell line was selected for subsequent experiments. Using ENCORI database, the putative target genes of the microRNA (miR) miR-6512-3p were predicted. Cells were then transfected with lentiviruses carrying short-hairpin-PAARH to interfere with PAARH expression. Subsequently, HepG2 liver cancer cells were transfected with a miR-6512-3p mimic and an inhibitor, and the expression levels of miR-6512-3p and the LIM and SH3 domain protein 1 (LASP1) in cells were assessed using RT-qPCR analysis. Cell proliferation was subsequently evaluated using colony formation assays, and immunofluorescence and western blotting were used to assess the expression level of LASP1 in transfected cells. The binding interaction between miR-6512-3p and LASP1 was further evaluated using a dual-luciferase reporter gene assay. Liver cancer cells were found to exhibit higher expression levels of PAARH compared with normal liver cells. Following PAARH interference, the expression level of miR-6512-3p was significantly increased, whereas that of LASP1 was significantly decreased, resulting in a reduction in cell proliferation. In liver cancer cells, miR-6512-3p overexpression led to a significant reduction in the LASP1 level and reduced proliferation, whereas suppressing miR-6512-3p led to a significant increase in LASP1 levels and increased proliferation. Additionally, the inhibition of miR-6512-3p caused the states of low LASP1 expression and reduced cell proliferation to be reversed. LASP1, a recently identified target gene of miR-6512-3p, was demonstrated to be suppressed by miR-6512-3p overexpression, thereby inhibiting liver cancer cell proliferation. Taken together, the findings of the present study demonstrate that the lncRNA PAARH may enhance liver cancer cell proliferation by engaging miR-6512-3p to target LASP1.

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“…Another study with a novel research concept suggested that miR-302 and GCNT3 can both regulate the ERK pathway and epithelialmesenchymal transition and could potentially be cancer treatment targets (28). Several basic studies have verified that mir-3619, a relatively newly discovered miRNA, can play a regulatory role in the occurrence and development of tumors through the regulatory axis proposed based on the ceRNA hypothesis (29)(30)(31). Nonetheless, the discovery of other modes of action of mir-3619 requires more effort.…”

Section: Discussionmentioning

confidence: 99%

Revealing potential immunotherapy targets through analysis of a ceRNA network in human colon adenocarcinoma

Li¹,

Zhu²,

Hou³

et al. 2021

Transl Cancer Res TCR

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Background: Microsatellite instability-high (MSI-H) is a special type of human colon adenocarcinoma (COAD) that responds well to immunotherapy. MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs), which are important members of competing endogenous RNAs (ceRNAs) networks, are involved in the tumorigenesis and development of MSI-H COAD. This study aimed to establish a ceRNA network for MSI in COAD to identify targets and prognostic markers that may explain the effects of immunotherapy.Methods: COAD sequencing data were extracted from The Cancer Genome Atlas (TCGA), after which differentially expressed miRNAs, lncRNAs, and mRNAs were determined according to microsatellite status.After building a network based on the ceRNA hypothesis, the relationships between microsatellite status and clinical features were explored. Biological processes in the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) databases were analyzed for specific miRNAs, lncRNAs, and mRNAs.Survival analysis was used to identify potential biomarkers.Results: Based on the inclusion criteria, a total of 363 COAD samples were obtained from TCGA. Strict screening criteria were used to identify differentially expressed RNAs in the MSI-H and microsatellite-stable groups, with 82 miRNAs, 1,280 lncRNAs, and 2121 mRNAs obtained (fold change >2, false discovery rate <0.01). Based on the RNA interaction mechanism, a miRNA-lncRNA-mRNA network was constructed, through which a subnetwork composed of 5 miRNAs was discovered. hsa-miR-31-5p, hsa-miR-302a-3p, hsa-miR-302b-3p, hsa-miR-302d-3p, hsa-miR-3619-5p and the RNAs interaction with them have the potential to become novel targets to change the effect of existing immunotherapy. GO and KEGG analyses showed that these differentially expressed miRNAs, lncRNAs, and mRNAs may play key roles in tumorigenesis, tumor development, and drug efficacy, with natural killer cells potentially becoming the next emerging targets for immunotherapy enhancement. Moreover, survival analysis identified 10 lncRNAs as potential survival markers.Conclusions: This study identified novel immunotherapy targets and revealed potential biomarkers for COAD according to microsatellite status.

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LncRNA NEAT1 Knockdown Inhibits Retinoblastoma Progression by miR-3619-5p/LASP1 Axis

Cited by 12 publications

References 24 publications

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

lncRNA PAARH impacts liver cancer cell proliferation by engaging miR‑6512‑3p to target LASP1

Revealing potential immunotherapy targets through analysis of a ceRNA network in human colon adenocarcinoma

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