Integrated analysis of lncRNA-miRNA-mRNA ceRNA network in squamous cell carcinoma of tongue

Zhou, Ruisheng; Zhang, Enxin; Qi-zhong, Sun; Ye, Zeng Jie; Liu, Jianwei; Zhou, Dajun; Tang, Ying

doi:10.1186/s12885-019-5983-8

Cited by 275 publications

(200 citation statements)

References 44 publications

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“…Recently, lncRNAs have been widely demonstrated to function as ceRNAs, and to directly interact with the mRNA-binding site in miRNAs to attenuate either the translational suppression or degradation of target mRNAs, thereby increasing the mRNA and protein levels of target genes. 41,62,63 To investigate whether SNHG7 acts as an miRNA sponge, bioinformatic prediction was performed, and the findings indicated that an miR-485-binding site is present in SNHG7. The luciferase reporter and RIP assays confirmed the direct interaction between SNHG7 and miR-485 in cervical cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…An increasing number of studies indicate that lncRNAs located in the cytoplasm exert their effects on human cancers by acting as a ceRNA for miRNAs. [39][40][41] To illustrate the oncogenic mechanisms of SNHG7 action on cervical cancer cells, we first determined the distribution of SNHG7 within HeLa and C-33A cells. The results suggested that SNHG7 was mainly located in the cytoplasm of HeLa and C-33A cells ( Figure 3A), implying that this lncRNA may serve as a ceRNA in cervical cancer cells.…”

Section: The Snhg7 Knockdown Inhibits the Malignant Characteristics Omentioning

confidence: 99%

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<p>Long Noncoding RNA SNHG7, a Molecular Sponge for microRNA-485, Promotes the Aggressive Behavior of Cervical Cancer by Regulating PAK4</p>

Wu¹,

Sui²,

Wang³

et al. 2020

OTT

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Purpose: A long noncoding RNA called small nucleolar RNA host gene 7 (SNHG7) is known to be a key regulator of biological processes in multiple human cancer types. In this study, our aims were to determine the expression status of SNHG7 in cervical cancer, to figure out the detailed roles of SNHG7 in cervical cancer cells, and to identify the mechanism underlying the activity of SNHG7 in cervical cancer. Methods: Reverse-transcription quantitative PCR was performed to measure SNHG7 expression in cervical cancer. A Cell Counting Kit-8 assay, flow-cytometric analysis, cell migration and invasion assays, and a tumor xenograft experiment were conducted to respectively determine the effects of SNHG7 on cervical cancer cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo. Results: SNHG7 was found to be markedly upregulated in cervical cancer tissues and cell lines. Higher SNHG7 expression significantly correlated with FIGO stage, lymph node metastasis, the depth of cervical invasion, and shorter overall survival in patients with cervical cancer. Functional experiments indicated that a SNHG7 knockdown attenuated proliferation, migration, and invasiveness and promoted apoptosis of cervical cancer cells in vitro. The SNHG7 knockdown also slowed tumor growth in vivo. Further investigation showed that SNHG7 acts as a competing endogenous RNA for microRNA-485 (miR-485) in cervical cancer cells, and the inhibitory actions of the SNHG7 knockdown on the malignant phenotype were reversed by miR-485 inhibition. P21-activated kinase 4 (PAK4) was identified as a direct target gene of miR-485 in cervical cancer, and PAK4 expression was promoted by SNHG7. Conclusion: SNHG7 functions as an oncogenic RNA in cervical cancer, competitively binds to miR-485, and thereby upregulates PAK4. This SNHG7-miR-485-PAK4 regulatory network may provide insights into the pathogenesis of cervical cancer, and can help in the identification of novel diagnostic and therapeutic approaches for cervical cancer.

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Section: Discussionmentioning

confidence: 99%

Section: The Snhg7 Knockdown Inhibits the Malignant Characteristics Omentioning

confidence: 99%

<p>Long Noncoding RNA SNHG7, a Molecular Sponge for microRNA-485, Promotes the Aggressive Behavior of Cervical Cancer by Regulating PAK4</p>

Wu¹,

Sui²,

Wang³

et al. 2020

OTT

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“…Accumulating evidence has suggested that lncRNAs may serve as ceRNAs to regulate the expression of miRs and mRNAs (25,26). Therefore, the present study aimed to elucidate the mechanism underlying the MIAT/miR-184 axis in NSCLC cells.…”

Section: Miat Promotes the Expression Of Sf1 By Sponging Mir-184 In Hmentioning

confidence: 97%

Knockdown of lncRNA MIAT inhibits proliferation and cisplatin resistance in non‑small cell lung cancer cells by increasing miR‑184 expression

Liu

Zhang

2019

Oncol Lett

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Accumulating evidence has demonstrated the important role of long non-coding RNA myocardial infarction-associated transcript (MIAT) in tumorigenesis as a potential oncogene. However, the function of MIAT in non-small cell lung cancer (NSCLC) has yet to be completely elucidated. The present study demonstrated that MIAT expression was significantly upregulated in NSCLC tissues, particularly in aggressive cases, and was highly associated with a poor prognosis. In addition, the upregulated expression of MIAT was observed in cisplatin (CDDP)-resistant H1299 cells. Knockdown of MIAT inhibited the proliferation of NSCLC cells and enhanced the sensitivity of NSCLC cells to CDDP in vitro and in vivo. Further functional analysis demonstrated that MIAT partially exerted its oncogenic effect by upregulating the expression of splicing factor 1 (SF1), by serving as a microRNA (miR)-184 sponge. In conclusion, the present study identified that MIAT functions as a competitive endogenous RNA of miR-184to modulate SF1 expression in NSCLC, which provides a novel insight into the potential therapeutic application of MIAT in NSCLC progression.

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“…A change in lncRNA expression has been identified in a variety of human cancer types, including gastric cancer (11), thyroid cancer (12), hepatocellular carcinoma (13) and TScc (14). Regarding TScc, recent studies have indicated that numerous lncRNAs are abnormally expressed in this type of tumor and act as either tumor-suppressors or oncogenic RNAs (15,16). The abnormal expression of lncRNAs may contribute toward the malignancy of TScc by affecting a number of malignant characteristics (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA PRNCR1 exerts oncogenic effects in�tongue squamous cell carcinoma in�vitro and in�vivo by sponging microRNA‑944 and thereby increasing HOXB5�expression

Zou

et al. 2020

Int J Mol Med

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A long non-coding RNA (lncRNA) called prostate cancer-associated non-coding RNA 1 (PRNCR1) serves crucial roles in the aggressive phenotypes of colorectal cancer and non-small cell lung cancer. However, there is little research on the expression profile, clinical value and detailed functions of PRNCR1 in tongue squamous cell carcinoma (TScc). The aim of the present study was to determine PRNCR1 expression in TScc and to examine the involvement of PRNCR1 in TScc progression. The molecular mechanisms behind the oncogenic effects of PRNCR1 in TScc cells were also investigated. PRNCR1 was revealed to be upregulated in TScc tumors and cell lines. The high PRNCR1 expression showed a significant correlation with tumor size, clinical stage, lymph node metastasis, and shorter overall survival times among patients with TScc. A PRNCR1-knockdown reduced TScc cell proliferation, migration and invasion, and increased apoptosis in vitro. Additionally, the PRNCR1-knockdown slowed down in vivo tumor growth of TScc cells. With regards to the mechanism, PRNCR1 acted as a competing endogenous RNA on microRNA-944 (miR-944) in TScc cells, and the effects of the PRNCR1-knockdown were reversed by an miR-944-knockdown. HOXB5 was validated as a direct target gene of miR-944 in TScc cells, and HOXB5 expression was found to be positively regulated by PRNCR1. Furthermore, resumption of HOXB5 expression reversed the tumor-suppressive actions of miR-944 in TScc cells. In conclusion, PRNCR1 acts as an oncogenic lncRNA in TScc through the upregulation of HOXB5 by sponging miR-944, thereby indicating a potential therapeutic target in TScc.

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Integrated analysis of lncRNA-miRNA-mRNA ceRNA network in squamous cell carcinoma of tongue

Cited by 275 publications

References 44 publications

<p>Long Noncoding RNA SNHG7, a Molecular Sponge for microRNA-485, Promotes the Aggressive Behavior of Cervical Cancer by Regulating PAK4</p>

<p>Long Noncoding RNA SNHG7, a Molecular Sponge for microRNA-485, Promotes the Aggressive Behavior of Cervical Cancer by Regulating PAK4</p>

Knockdown of lncRNA MIAT inhibits proliferation and cisplatin resistance in non‑small cell lung cancer cells by increasing miR‑184 expression

Long non‑coding RNA PRNCR1 exerts oncogenic effects in�tongue squamous cell carcinoma in�vitro and in�vivo by sponging microRNA‑944 and thereby increasing HOXB5�expression

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