Long non-coding RNA 520 is a negative prognostic biomarker and exhibits pro-oncogenic function in nasopharyngeal carcinoma carcinogenesis through regulation of miR-26b-3p/USP39 axis

Xie, Tao; Pi, Guoliang; Yang, Bin; Ren, Hui; Yu, Jing; Ren, Qingrong; Zhou, Xiaoyi; Hu, Desheng; Zhang, Haiyuan; Zhang, Hao; Qu, Zhipeng; Hu, Liu; Liu, Ying; Zhou, Fuxing

doi:10.1016/j.gene.2019.02.093

Cited by 22 publications

(21 citation statements)

References 54 publications

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“…The present study confirmed the high expression of LINC00520 in glioma tissues and in glioma cells, and LINC00520 promoted the malignant biological behaviors of glioma cells. A similar study described the expression of LINC00520 in nasopharyngeal carcinoma, and the relationship between LINC00520 overexpression and the proliferation of nasopharyngeal carcinoma cells . LINC00520 also acts as a tumor promoting factor in renal cell carcinoma, and promotes the development of renal cell carcinoma .…”

Section: Discussionmentioning

confidence: 84%

“…A similar study described the expression of LINC00520 in nasopharyngeal carcinoma, and the relationship between LINC00520 overexpression and the proliferation of nasopharyngeal carcinoma cells. 43 LINC00520 also acts as a tumor promoting factor in renal cell carcinoma, and promotes the development of renal cell carcinoma. 44 Therefore, LINC00520 could be an oncogene in glioma, nasopharyngeal carcinoma, and renal cell carcinoma.…”

Section: Discussionmentioning

confidence: 99%

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Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

et al. 2020

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Upstream ORF (uORF) is a translational initiation element located in the 5′UTR of eukaryotic mRNAs. Studies have found that uORFs play an important regulatory role in many diseases. Based on The Cancer Genome Atlas database, the results of our experiments and previous research evidence, we investigated transcription factor AP‐4 (TFAP4) and its uORF, LIM and SH3 protein 1 (LASP1), long noncoding RNA 00520 (LINC00520), and microRNA (miR)‐520f‐3p as candidates involved in glioma malignancy, which is a poorly understood process. Both TFAP4‐66aa‐uORF and miR‐520f‐3p were downregulated, and TFAP4, LASP1, and LINC00520 were highly expressed in glioma tissues and cells. TFAP4‐66aa‐uORF or miR‐520f‐3p overexpression or TFAP4, LASP1, or LINC00520 knockdown inhibited glioma cell proliferation, migration, and invasion, but promoted apoptosis. TFAP4‐66aa‐uORF inhibited the translation of TFAP4 by binding to the TFAP4 mRNA. MicroRNA‐520f‐3p inhibited TFAP4 expression by binding to its 3′UTR. However, LINC00520 could promote the expression of TFAP4 by competitively binding to miR‐520f‐3p. In addition, TFAP4 transcriptionally activated LASP1 and LINC00520 expression by binding to their promoter regions, forming a positive feedback loop of TFAP4/LINC00520/miR‐520f‐3p. Our findings together indicated that TFAP4‐66aa‐uORF inhibited the TFAP4/LINC00520/miR‐520f‐3p feedback loop by directly inhibiting TFAP4 expression, subsequently leading to inhibition of glioma malignancy. This provides a basis for developing new therapeutic approaches for glioma treatment.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

et al. 2020

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“…35 Significantly, the mediated effect of AKT signalling in the regulation of RGC-32 has been referred, for example, complement activation induces generation of C5a, as an important immune mediator, and then, activates RGC-32 to promote cell proliferation, which is regulated by Akt activation in breast cancer. 27 45 melanoma, 46 nasopharyngeal carcinoma, 56 cervical cancer, 40 bladder cancer, 44 colorectal cancer, 43,57 breast cancer, 41 pancreatic cancer 58 and lung cancer. 59 Pronouncedly, Baghaei et al has pointed out that miR-26b emerges as a potential tumour suppressor in oral squamous cell carcinoma, via regulating target protein.…”

Section: Discussionmentioning

confidence: 99%

Oncogenic gene RGC‐32 is a direct target of miR‐26b and facilitates tongue squamous cell carcinoma aggressiveness through EMT and PI3K/AKT signalling

Yang

Chen

et al. 2020

Cell Biochemistry & Function

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Growing data have recognized the significance of Response Gene to Complement (RGC)-32 in numerous tumour developments. Notwithstanding, the functional role and underlying mechanism of it in tongue squamous cell carcinoma (TSCC) remain enigmatic. Here, to identify the impact of RGC-32 in TSCC, its expression in multiple TSCC cells was measured and loss-of-function experiments in cell lines were performed to illuminate the function of it induced TSCC progression, via si-RNA knockdown, CCK-8, colony formation, wound-healing, transwell, flow cytometry and western blot assays. To clarify potential mechanism, expressions of hallmarks in epithelial-mesenchymal transition (EMT) process and PI3K/AKT signalling were assessed, and the upstream miR regulator of RGC-32 was predicted and verified by applying bioinformatic approaches and dual-luciferase reporter assay, respectively. Finally, the rescue experiments were applied to better elucidate the effect of miR-26b/RGC-32 axis in TSCC behaviours. As a result, RGC-32 was upregulated in TSCC cells and knocking down of it abrogated cell proliferation, trans-migration and invasion, whilst promoted apoptosis in TSCC, which was regulated through repressing EMT and inactivation of PI3K/AKT signalling. Subsequently, miR-26b was predicted and identified as an upstream regulator of RGC-32, and the pro-tumorigenic effect of RGC-32 was reversed by miR-26b overexpression. Collectively, our results demonstrated that RGC-32 facilitated TSCC progression, which was modulated by activations of PI3K/AKT pathway and EMT process, and reduction of its negative regulator of miR-26b. These findings highlight a novel role of miR-26b/RGC-32 axis in TSCC and underlying mechanism, encouraging a potent usage in TSCC treatment. Significance of the study: We first uncovered that Response Gene to Complement-32 played a significantly pro-tumorigenic role in tongue squamous cell carcinoma (TSCC), which was closely regulated by downregulation of miR-26b and activations of epithelial-mesenchymal transition process and PI3K/AKT signalling. These findings contribute to better understand the molecular mechanism in carcinogenesis of TSCC, and shed some light on promising strategy for TSCC therapeutics.

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“…The upregulation of LINC00520 expression might play an important biological role in the metastasis of laryngeal squamous cell carcinoma. The expression of LINC00520 was upregulated in primary nasopharyngeal carcinoma . In addition, the level of LINC00520 was significantly increased in renal cell carcinoma .…”

Section: Introductionmentioning

confidence: 93%

“…The expression of LINC00520 was upregulated in primary nasopharyngeal carcinoma. 17 In addition, the level of LINC00520 was significantly increased in renal cell carcinoma. 18 LINC00520 promoted the migration of BC cells induced by Src, STAT3, and PI3K and played a functional role in BC.…”

Section: Introductionmentioning

confidence: 97%

Characterization of lncRNA LINC00520 and functional polymorphisms associated with breast cancer susceptibility in Chinese Han population

Guo

Peng

et al. 2020

Cancer Medicine

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Background The aim was to evaluate the association between the LINC00520 genetic polymorphisms and breast cancer (BC) susceptibility. Methods Nine single‐nucleotide polymorphisms (SNPs) on LINC00520 genotyping were performed in 504 BC patients and 505 cancer‐free controls in Chinese Han population to study the relationship between LINC00520 polymorphism and BC susceptibility. qRT‐PCR and luciferase tests were used to explore how rs12880540 affected the expression of LINC00520. Results The genotype GG (OR:3.58, 95%CI:1.32‐9.69) in rs8012083 increased the risk of triple‐negative BC. The genotype GG (OR:0.31, 95%CI:0.14‐0.69) in rs8012083, the genotype AA (OR:2.74, 95%CI:1.01‐7.42) in rs2152275, and genotype TG (OR:1.62, 95%CI:1.04‐2.52) in rs12880540 were associated with HER‐2 status. The dominant (OR:0.65, 95%CI:0.45‐0.95) and overdominant genetic model (OR:0.67, 95%CI:0.46‐0.98) consistently showed that rs11622641 T was significantly associated with lower risk of BC. Similarly, the recessive genetic model (OR:1.57, 95%CI:1.07‐2.30) of rs12880540 and the dominant (OR:1.62, 95%CI:1.24‐2.11) and overdominant (OR:1.56, 95%CI:1.19‐2.03) genetic model of rs2152278 may increase the risk of BC. The relative expression of LINC00520 increased linearly with the increase in the number of rs12880540 mutations. rs12880540 alleles were due to the interaction between LINC00520 and miR‐3122 at T, but the mutation of rs12880540 G > T had no effect on the binding ability of LINC00520 and miR‐3122. Conclusion A genetic variant of rs8012083 in LINC00520 may be used as a biomarker for triple‐negative BC after further evaluation of diagnostic tests. The genetic variant of LINC00520 was related to the susceptibility of BC, and rs12880540 might affect the corresponding mRNA expression of lncRNA LINC00520.

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Long non-coding RNA 520 is a negative prognostic biomarker and exhibits pro-oncogenic function in nasopharyngeal carcinoma carcinogenesis through regulation of miR-26b-3p/USP39 axis

Cited by 22 publications

References 54 publications

Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

Oncogenic gene RGC‐32 is a direct target of miR‐26b and facilitates tongue squamous cell carcinoma aggressiveness through EMT and PI3K/AKT signalling

Characterization of lncRNA LINC00520 and functional polymorphisms associated with breast cancer susceptibility in Chinese Han population

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