Up-regulated long non-coding RNA ILF3-AS1 indicates poor prognosis of nasopharyngeal carcinoma and promoted cell metastasis

Yang, Xuewen; Lin, Feng; Gao, Feng

doi:10.1177/1724600820955199

Cited by 10 publications

(6 citation statements)

References 34 publications

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“…Based on RIP assay, miR-320a was screened out for further study. Dysregulated miR-320a has been determined to play a critical role in various cancers, such as cervical cancer [38], melanoma [39], nasopharyngeal carcinoma [40] and retinoblastoma [41]. In keeping with the findings of prior studies, our results showed that compared with normal brain tissues and normal human astrocytes, miR-320a was downregulated in glioma tissues and cell lines, respectively.…”

Section: Discussionsupporting

confidence: 89%

“…Glioma, which accounts for approximately 40-50% of all central nervous system (CNS) tumours, is the most common primary CNS tumour in adults [1,2]. The clinical symptoms of glioma primarily include headache, vomiting, epilepsy, loss of neurological function, disturbance of consciousness and cerebral hernia caused by the tumour mass effect, which seriously threaten the life of glioma patients [3].…”

Section: Introductionmentioning

confidence: 99%

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FGF14-AS2 accelerates tumorigenesis in glioma by forming a feedback loop with miR-320a/E2F1 axis

Zhang¹,

Gu²,

Zhang³

et al. 2021

J. Cancer

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Glioma is the most common primary tumour in the central nervous system in adults, and at present, there is no effective treatment to cure this malignancy. Long noncoding RNAs (lncRNAs) are closely related to tumour progression and have attracted increasing attention in tumour research. However, the role of lncRNA FGF14-AS2 in glioma tumorigenesis has not been determined. In the present study, we found that FGF14-AS2 expression was significantly elevated in glioma tissues and was associated with poor survival in glioma patients. Silencing FGF14-AS2 inhibited the proliferation, migration and invasion ability of glioma cells. In vivo assay showed that silencing FGF14-AS2 led to inhibition of tumour growth. In addition, FGF14-AS2 was observed to promote glioma progression via the miR-320a/E2F1 axis. Moreover, E2F1 could bind to the promoter region of FGF14-AS2, thereby enhancing FGF14-AS2 expression. In conclusion, FGF14-AS2 could accelerate tumorigenesis of glioma by forming a feedback loop with the miR-320a/E2F1 axis which suggested that FGF14-AS2 could serve as a therapeutic target for glioma.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

FGF14-AS2 accelerates tumorigenesis in glioma by forming a feedback loop with miR-320a/E2F1 axis

Zhang¹,

Gu²,

Zhang³

et al. 2021

J. Cancer

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“…Yang et al indicated that ILF3-AS1 was elevated in nasopharyngeal carcinoma and that accelerated cell metastasis of nasopharyngeal carcinoma patients [15]. Chen et al revealed that ILF3-AS1 was signi cantly increased in melanoma tissues and ILF3-AS1 silence restrained melanoma cell growth and metastasis [16].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of LncRNA ILF3-AS1 restrained NSCLC development through miR-185-5p/ING4 axis

Li,

Song,

Fang

2023

Preprint

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LncRNA ILF3-AS1 was abnormally expressed in several cancers. However, the relationship of ILF3-AS1 and non-small cell lung cancer (NSCLC) still unknown. Now, our research endeavored to characterize the expression and function of ILF3-AS1 in NSCLC, so as to study its related mechanism. The differential level of ILF3-AS1 in NSCLC were detected. The relation of miR-185-5p with ILF3-AS1 and ING4 was predicted by bioinformatics online tool and further verified. The influence of ILF3-AS1 and miR-185-5p inhibitor on cell biological function were detected by a series of tests. The changes of tumor volume and weight intervened by ILF3-AS1 up-regulation and miR-185-5p depletion were monitored in mice. ILF3-AS1 was abnormally down-expressed not only in NSCLC tissues, but also in NSCLC cells. ILF3-AS1 overexpression can inhibit the viability of NSCLC cells, reduce the number of migrating and invading cells, and enhance the apoptosis, which was reversed by miR-185-5p mimics. There were direct interactions between miR-185-5p, ILF3-AS1, and ING4. Tumor inhibition was observed in mice transplanted with H1299 transfected by pcDNA3.1-ILF3-AS1 and miR-185-5p inhibitor. ILF3-AS1 modulated NSCLC progress through targeting miR-185-5p/ING4 axis.

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“…For example, ILF3-AS1 promoted cell metastasis in nasopharyngeal carcinoma, and its high expression indicated poor prognosis. 15 In gastric cancer, ILF3-AS1 promoted gastric cancer progression through the miR-29a/PTBP1 pathway. 16 In osteosarcoma, ILF3-AS1 regulated SOX5 expression through miR-212.…”

Section: Discussionmentioning

confidence: 99%

LncRNA ILF3-AS1 Promotes the Progression of Colon Adenocarcinoma Cells Through the miR-619-5p/CAMK1D Axis

Liu¹,

Li²

2021

OTT

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Introduction: Colon adenocarcinoma (COAD) is the third most common tumor of the digestive tract. Recent studies reported that lncRNA's abnormal expression might play a vital role in the occurrence and development of COAD. Methods: In the present study, we investigated the expression of ILF3-AS1 in COAD cell lines, human normal colon epithelial cell line, patient tumor tissues and adjacent normal tissues by real-time quantitative PCR (RT-qPCR). Small interfering RNAs (siRNAs) were transfected into COAD cells to inhibit the expression of ILF3-AS1. The effects of ILF3-AS1 on cell proliferation, migration, invasion and apoptosis were measured by CCK-8 assay, transwell migration and invasion assay, and flow cytometry apoptosis assay, respectively. The direct binding of ILF3-AS1 and miR-619-5p/CAMK1D was validated by the luciferase reporter assay. The expression of CAMK1D and epithelial-mesenchymal transformation (EMT)-related proteins was detected by Western Blot analysis. Besides, in vivo experiments were conducted to demonstrate the oncogenic role of ILF3-AS1 in COAD. Results: The results showed that the expression of ILF3-AS1 was significantly higher in COAD tissue than in normal adjacent samples, and this conclusion was confirmed in the available public datasets. After ILF3-AS1 knockdown, the proliferation of COAD cell lines SW480 and HT29 was significantly inhibited. At the same time, the apoptosis was increased, and the invasion and migration abilities were decreased. After further exploring the mechanisms, we found that ILF3-AS1 serves as a competitive endogenous RNA of mir-619-5p. It can bind to mir-619-5p and reduce its expression, thus regulating the target gene CAMK1D. In addition, we found that high expression of ILF3-AS1 was significantly associated with tumor grade, tumor size, and distant metastasis in COAD samples. In vivo experiments confirmed that ILF3-AS1 promotes tumor growth in COAD models. Conclusion: The present study demonstrated that ILF3-AS1 plays an oncogenic role in COAD through regulating the miR-619-5p/CAMK1D axis, and inhibition of ILF3-AS1 may pave the way for COAD treatment.

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Up-regulated long non-coding RNA ILF3-AS1 indicates poor prognosis of nasopharyngeal carcinoma and promoted cell metastasis

Cited by 10 publications

References 34 publications

FGF14-AS2 accelerates tumorigenesis in glioma by forming a feedback loop with miR-320a/E2F1 axis

FGF14-AS2 accelerates tumorigenesis in glioma by forming a feedback loop with miR-320a/E2F1 axis

Overexpression of LncRNA ILF3-AS1 restrained NSCLC development through miR-185-5p/ING4 axis

LncRNA ILF3-AS1 Promotes the Progression of Colon Adenocarcinoma Cells Through the miR-619-5p/CAMK1D Axis

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