LncRNA ZFAS1 promotes proliferation and migration and inhibits apoptosis in nasopharyngeal carcinoma via the PI3K/AKT pathway in vitro

Wang, Xiaoqiong; Qi, Jin; Wang, Xue; Chen, Wubing; Cai, Zhenzhai

doi:10.3233/cbm-182080

Cited by 23 publications

(14 citation statements)

References 48 publications

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“…15 With using Lipofectamine 3000 (Invitrogen, Carlsbad, CA, USA), siRNA for lncRNA ILF3-AS1 (siRNA-lncRNA ILF3-AS1) or negative control (siRNA-NC) was added to each well at a concentration of 50 nmol/L. 16,17 The siRNAs are synthesized by the GenScript Corporation (Nanjing, China). The siRNA-lncRNA ILF3-AS1 sequence is: 5′-TCGCCCTGAGTA CGTTAGCGGAAAT-3′.…”

Section: Cells Lines and Cell Transfectionmentioning

confidence: 99%

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

2020

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Background: Long non-coding RNAs (lncRNAs) have been confirmed to participate in the regulation of nasopharyngeal carcinoma. Here, we endeavored to explore the character of lncRNA ILF3-AS1 in the nasopharyngeal carcinoma and its function. Methods: A total of 68 nasopharyngeal carcinoma tissues and adjacent normal nasopharyngeal tissues were collected. Expressions of lncRNA ILF3-AS1 in these tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between the expression level of lncRNA ILF3-AS1 and clinical pathological characteristics was analyzed. Inhibition of lncRNA ILF3-AS1 was done using small interference RNA. Results: lncRNA ILF3-AS1 expression was significantly up-regulated in the 68 nasopharyngeal carcinoma tissue samples compared to their adjacent normal tissue samples. Increased lncRNA ILF3-AS1 level was related to the advanced tumor node metastasis stage and the metastasis of nasopharyngeal carcinoma. Also, increased lncRNA ILF3-AS1 indicated poor prognosis of nasopharyngeal carcinoma patients. Inhibition of lncRNA ILF3-AS1 reduced proliferation, invasion and migration of nasopharyngeal carcinoma cells. MicroRNA-320a (miR-320a) was determined as a direct target for lncRNA ILF3-AS1 in nasopharyngeal carcinoma. Furthermore, lncRNA ILF3-AS1 could sponge miR-320a to promote BMI1 expression. The expression of BMI1 was significantly inhibited by the down-regulation of lncRNA ILF3-AS1. Conclusions: For the first time, we demonstrated that lncRNA ILF3-AS1 was markedly over-expressed in nasopharyngeal carcinoma tissues and cells. Elevated lncRNA ILF3-AS1 expression was correlated with severe cancer stage and poor prognosis. lncRNA ILF3-AS1 could promote proliferation, invasion, and migration of cells, which might indicate a novel target site for the future diagnosis and therapy of nasopharyngeal carcinoma.

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Section: Cells Lines and Cell Transfectionmentioning

confidence: 99%

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

2020

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“…Long non-coding RNAs (lncRNAs) are a group of transcribed RNA molecules with a length of over 200 nucleotides. Accumulating evidence demonstrated that dysregulated lncRNAs, such as DANCR, SMAD5-AS1, LINC00460 and ZFAS1, have been broadly implicated in the NPC development and progression [8][9][10][11]. Family with sequence similarity 225 member B (FAM225B), also known as LINC00256B, is a newly discovered lncRNA located on chromosome 9q32.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA FAM225B facilitates proliferation and metastasis of nasopharyngeal carcinoma cells by regulating miR-613/CCND2 axis

Dai¹,

Shi²,

Hu³

et al. 2021

Bosn J of Basic Med Sci

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Growing evidence has suggested that abnormally expressed long non-coding RNAs (lncRNAs) play critical regulatory roles in nasopharyngeal carcinoma (NPC) pathogenesis. Family with sequence similarity 225 member B (FAM225B) is a novel lncRNA that has been implicated in several human cancers, yet its role in the context of NPC remains largely unclear. The aim of this study was to determine the expression level of FAM225B and its clinical significance in NPC patients. We observed a remarkable increase of FAM225B in NPC tissues and cell lines compared with controls. Also, highly expressed FAM225B was closely correlated with advanced TNM stage, distant metastasis, and poor overall survival. Interestingly, loss-of-function analysis revealed that FAM225B knockdown significantly inhibited tumor growth in vitro and in vivo, and decreased the migratory and invasive capacity of NPC cells. Mechanically, FAM225B functioned as an endogenous sponge by competing for miR-613 binding to up-regulate CCND2 expression. More importantly, rescue experiments further demonstrated that the suppressive impacts of FAM225B knockdown on cell proliferation, migration and invasion were significantly reversed after CCND2 overexpression. Taken all together, these findings highlight FAM225B as an oncogene that promotes NPC proliferation and metastasis through miR-613/CCND2 axis.

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“…lncRNAs have been discovered to serve roles in inhibiting or promoting the development of cancer by influencing carcinogenic molecules to regulate cancer-related progression. For example, lncRNA ZFAS1 was reported to accelerate the proliferation of NPC cells via the activation of the PI3K/AKT signaling pathway ( 25 ). Jia et al ( 15 ) also demonstrated that lncRNA PXN-AS1-L promoted the proliferation, migration and invasion of NPC cells through upregulating the expression levels of suppressor APC domain-containing protein 2.…”

Section: Discussionmentioning

confidence: 99%

KIF9‑AS1 promotes nasopharyngeal carcinoma progression by suppressing miR‑16

You

Wang

2020

Oncol Lett

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Long non-coding RNAs (lncRNAs) have been reported to serve a crucial role in the progression of nasopharyngeal carcinoma (NPC); however, the underlying molecular mechanisms of lncRNA KIF9-AS1 in the tumorigenesis of NPC remains poorly understood. Reverse transcription-quantitative PCR was used to analyze the expression levels of KIF9-AS1 and microRNA (miR)-16, and Cell Counting Kit-8, wound healing and Transwell assays were used to determine the cell viability, invasion and migration, respectively, of NPC cells. In addition, a dual-luciferase reporter assay was used to analyze the direct interaction between KIF9-AS1 and miR-16. NPC stage was classified according to the seventh edition of the AJCC staging system. The results revealed that KIF9-AS1 expression levels were upregulated in NPC tissues and cell lines. In addition, miR-16 was demonstrated to directly interact with KIF9-AS1 and inhibit KIF9-AS1 expression levels, whereas the miR-16 inhibitor rescued the effects of the KIF9-AS1-knockdown in NPC cells. Furthermore, the expression levels of KIF9-AS1 were upregulated, while those of miR-16 were downregulated in NPC tissues. Notably, the expression levels of KIF9-AS1 were observed to be significantly more upregulated in advanced tumors (III–IV vs. I–II) and patients with high KIF9-AS1 expression levels exhibited a worse prognosis. In conclusion, the findings of the present study suggested that KIF9-AS1 may promote the progression of NPC by targeting miR-16, thus KIF9-AS1 may be a novel molecular target for NPC therapy.

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LncRNA ZFAS1 promotes proliferation and migration and inhibits apoptosis in nasopharyngeal carcinoma via the PI3K/AKT pathway in vitro

Cited by 23 publications

References 48 publications

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

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

Long noncoding RNA FAM225B facilitates proliferation and metastasis of nasopharyngeal carcinoma cells by regulating miR-613/CCND2 axis

KIF9‑AS1 promotes nasopharyngeal carcinoma progression by suppressing miR‑16

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