Prader–Willi region non-protein coding RNA 1 suppressed gastric cancer growth as a competing endogenous RNA of miR-425-5p

Chen, Zihao; Ju, Hongping; Yu, Shan; Zhao, Ting; Jing, Xiaojie; Li, Ping; Jia, Jizeng; Li, Nan; Tan, Bibo; Li, Yong

doi:10.1042/cs20171588

Cited by 30 publications

(23 citation statements)

References 39 publications

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“…Recently, it was reported PWRN1 acted as an active factor in suppressing human gastric cancer cell growth. 19 However, to the best of our knowledge, discovery in the present study is the first one to report the functional mechanism of PWRN1 in human GBM.…”

Section: Discussionmentioning

confidence: 68%

“…In recent decades, strong evidence has demonstrated that lncRNAs may by aberrantly deregulated in human GBM tumors and closely associated with cancer patients' prognosis, thus making them potential candidates for diagnostic biomarkers or therapeutic targets for GBM. 13,14 In the present study, we suspected lncRNA of PWRN1, which has been shown to be dysregulated in several types of human cancers, [19][20][21]25 is also aberrantly expressed in human GBM, and functionally involved in GBM cell regulation. Based on this hypothesis, we used a systemic approach to assess the expression profile and possible regulatory mechanisms of PWRN1in GBM.…”

Section: Discussionmentioning

confidence: 72%

“…It is worth noting that, in human gastric cancer, PWRN1 was acting through miR-425-5p/p53 signaling feedback loop to modulate tumor cell growth and metastasis. 19 Thus, it is possible that PWRN1 may activate/inhibit other epigenetic signaling pathways, rather than hsa-miR-21-5p, to regulate cancer cell in GBM.…”

Section: Discussionmentioning

confidence: 99%

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PWRN1 Suppressed Cancer Cell Proliferation and Migration in Glioblastoma by Inversely Regulating hsa-miR-21-5p

Jiang¹,

Wang²,

Lü³

2020

CMAR

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To evaluate the expression and function of long noncoding RNA (lncRNA) Prader-Willi region non-protein coding RNA 1 (PWRN1) in human glioblastoma (GBM). Materials and Methods: QRT-PCR was applied to assess PWRN1 expression in human GBM tumors and GBM cell lines. PWRN1 was overexpressed by lentiviral infection in LN-229 and U-251 cells to evaluate its effect on GBM cell proliferation and migration in vitro, and xenograft in vivo. The endogenously competing target of PWRN1, human microRNA-21-5p (hsa-miR-21-5p) was evaluated by dual-luciferase activity assay and qRT-PCR. Also, hsa-miR-21-5p was upregulated in PWRN1-overexpressed GBM cells to evaluate the functional involvement of hsa-miR-21-5p in PWRN1-mediated GBM cell proliferation and migration. Results: PWRN1 was downregulated in both human GBM tumors and GBM cell lines. In LN-229 and U-251, PWRN1 overexpression suppressed cancer cell proliferation and migration in vitro, and xenograft growth in vivo. Hsa-miR-21-5p was demonstrated to be the downstream competing target of PWRN1 in GBM. Conversely, upregulating hsa-miR-21-5p in LN-229 and U-251 cells reversed the tumor-suppressing effects of PWRN1 overexpression. Conclusion: PWRN1 is markedly downregulated in GBM. Overexpressing PWRN1 has tumor inhibitory effect on GBM cells, likely via reversely suppressing the expression of tumor oncogenic factor of hsa-miR-21-5p.

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Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 72%

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PWRN1 Suppressed Cancer Cell Proliferation and Migration in Glioblastoma by Inversely Regulating hsa-miR-21-5p

Jiang¹,

Wang²,

Lü³

2020

CMAR

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“…Recently, it was reported that DLEU2 was involved in several types of cancer and DLEU2 exon 9 was an independent marker of poor prognosis in patients with esophageal adenocarcinoma (31). Aberrant expression levels of TCL6 were involved in clear cell renal carcinoma by regulating the PI3K/AKT pathway and PWRN1 inhibits gastric cancer cell proliferation and metastasis via p53 signaling pathway (32,33).…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of prognosis-related long non-coding RNAs in invasive breast carcinoma

Yin

et al. 2020

Oncol Lett

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Breast cancer is one of the most common types of cancer among women worldwide and needs more sensitive prognostic biomarkers to improve its treatment. In the present study, differentially expressed long non-coding RNAs (lncRNAs) in invasive breast carcinoma from The Cancer Genome Atlas and cBioPortal database were investigated, identifying 292 differentially expressed lncRNAs in 1,100 cases. By analyzing the overall survival rate, 10 lncRNAs were significantly correlated with poor prognosis. To explore the underlying molecular mechanisms of the 10 prognosis-related lncRNAs, bioinformatic methods were used to predict the potential target miRNAs, mRNAs and proteins, and to construct a lncRNA-miRNA-mRNA regulatory network and lncRNA-protein interaction network. Finally, the functions of the target genes and proteins were insvestigated using Gene Ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analyses. The results showed that these 10 lncRNAs could be novel prognostic markers for invasive breast carcinoma and the present study aimed to provide novel insight into the diagnosis and treatment of breast cancer.

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“…Wawrzik et al (107) hypothesized that the action of PWRN1 on the imprinting mechanism may be indirect through keeping the paternal allele in an open chromatin configuration, allowing access to transcription factors (107). The main limitation for further confirmation studies is the lack of gene orthology in mice (108)(109)(110).…”

Section: Genotype-phenotype Relationships In Prader-willi Syndromementioning

confidence: 99%

Genotype-Phenotype Relationships and Endocrine Findings in Prader-Willi Syndrome

Costa¹,

Ferreira²,

Cintra³

et al. 2019

Front. Endocrinol.

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Prader-Willi syndrome (PWS) is a complex imprinting disorder related to genomic errors that inactivate paternally-inherited genes on chromosome 15q11-q13 with severe implications on endocrine, cognitive and neurologic systems, metabolism, and behavior. The absence of expression of one or more genes at the PWS critical region contributes to different phenotypes. There are three molecular mechanisms of occurrence: paternal deletion of the 15q11-q13 region; maternal uniparental disomy 15; or imprinting defects. Although there is a clinical diagnostic consensus criteria, DNA methylation status must be confirmed through genetic testing. The endocrine system can be the most affected in PWS, and growth hormone replacement therapy provides improvement in growth, body composition, and behavioral and physical attributes. A key feature of the syndrome is the hypothalamic dysfunction that may be the basis of several endocrine symptoms. Clinical and molecular complexity in PWS enhances the importance of genetic diagnosis in therapeutic definition and genetic counseling. So far, no single gene mutation has been described to contribute to this genetic disorder or related to any exclusive symptoms.Here we proposed to review individually disrupted genes within the PWS critical region and their reported clinical phenotypes related to the syndrome. While genes such as MKRN3, MAGEL2, NDN, or SNORD115 do not address the full spectrum of PWS symptoms and are less likely to have causal implications in PWS major clinical signs, SNORD116 has emerged as a critical, and possibly, a determinant candidate in PWS, in the recent years. Besides that, the understanding of the biology of the PWS SNORD genes is fairly low at the present. These non-coding RNAs exhibit all the hallmarks of RNA methylation guides and can be incorporated into ribonucleoprotein complexes with possible hypothalamic and endocrine functions. Also, DNA conservation between SNORD sequences across placental mammals strongly suggests that they have a functional role as RNA entities on an evolutionary basis. The broad clinical spectrum observed in PWS and the absence of a clear genotype-phenotype specific correlation imply that the numerous genes involved in the syndrome have an additive deleterious effect on different phenotypes when deficiently expressed.

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Prader–Willi region non-protein coding RNA 1 suppressed gastric cancer growth as a competing endogenous RNA of miR-425-5p

Cited by 30 publications

References 39 publications

<p>PWRN1 Suppressed Cancer Cell Proliferation and Migration in Glioblastoma by Inversely Regulating hsa-miR-21-5p</p>

<p>PWRN1 Suppressed Cancer Cell Proliferation and Migration in Glioblastoma by Inversely Regulating hsa-miR-21-5p</p>

Bioinformatics analysis of prognosis-related long non-coding RNAs in invasive breast carcinoma

Genotype-Phenotype Relationships and Endocrine Findings in Prader-Willi Syndrome

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