p53‐induced long non‐coding RNA PGM5‐AS1 inhibits the progression of esophageal squamous cell carcinoma through regulating miR‐466/PTEN axis

Zhao, Zhihua; Wang, Weiwei; Niu, Lihua; Zhang, Jianying; Jiang, Guozhong

doi:10.1002/iub.2069

Cited by 20 publications

(13 citation statements)

References 37 publications

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“…HCC is one of the malignant diseases which has threatened the health of human, and miRNA dysfunction has been found as a key cause of cancer formation [ 15 ]. MiR-466 locates on chromosome 3, and several studies have indicated that miR-466 is significantly downregulated in some tumor cells and involves the regulations of the proliferation and invasion of the tumors [ 16 ]. In this study, the expression levels of miR-466 in HCC tissues and cell lines were investigated, and the effects of miR-466 on the phenotype of HCC cells such as proliferation, invasion, and apoptosis were also explored.…”

Section: Discussionmentioning

confidence: 99%

MiR-466 Inhibits the Progression of Severe Hepatocellular Carcinoma via Regulating FMNL2-Mediated Activation of NF-κB and Wnt/β-Catenin Pathways

2021

Journal of Oncology

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Hepatocellular carcinoma (HCC) has threatened the health of humans, and some evidence has indicated that miR-466 involves the progressions of some cancers. This study focused on the role of miR-466 in the formation and development of HCC. The expression levels of miR-466 in the tissues of patients and HCC cell lines were measured by qRT-PCR, and CCK-8, transwell assay, and flow cytometry assay were used to observe the functions of miR-466 on the HCC cells. Moreover, the miRNA databases, dual-luciferase reporter assay, and Western blot were used for the investigation of the regulation mechanism of miR-466 on HCC cells. The results showed that miR-466 was significantly downregulated in HCC tissues and cell lines, and inhibited proliferation, invasion, and high apoptosis were found in HCC cells when miR-466 was overexpressed. The results confirmed that FMNL2 was a target of miR-466, and increased FMNL2 could reverse the effects of miR-466 on the phenotype of HCC cells. Besides, it was also found that miR-466 was involved in the regulation of NF-κB and Wnt/β-catenin pathways in HCC cells via targeting FMNL2. In conclusion, the results of this study suggest that miR-466 regulates the activities of NF-κB and Wnt/β-catenin pathways to inhibit the progression of HCC cells via targeting FMNL2.

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Section: Discussionmentioning

confidence: 99%

MiR-466 Inhibits the Progression of Severe Hepatocellular Carcinoma via Regulating FMNL2-Mediated Activation of NF-κB and Wnt/β-Catenin Pathways

2021

Journal of Oncology

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“…The lncRNA PGM5-AS1 has been limitedly studied (n=4 in PubMed under 'PGM5-AS1'). Evidence suggests PGM5-AS1 suppresses esophageal squamous cell carcinoma by facilitating PTEN actions though sponging miR-466 (224). Apart from SNHG1, CRNDE, PART1 and PGM5-AS1, the others in the 7-lncRNA panel (Table VI) have not yet been reported, at least to the best of our knowledge…”

Section: Gene Expression-based Biomarkersmentioning

confidence: 99%

Assessment of biochemical recurrence of prostate cancer (Review)

Lin

Kapoor

et al. 2019

Int J Oncol

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The assessment of the risk of biochemical recurrence (BCR) is critical in the management of males with prostate cancer (PC). Over the past decades, a comprehensive effort has been focusing on improving risk stratification; a variety of models have been constructed using PC-associated pathological features and molecular alterations occurring at the genome, protein and RNA level. Alterations in RNA expression (lncRNA, miRNA and mRNA) constitute the largest proportion of the biomarkers of BCR. In this article, we systemically review RNA-based BCR biomarkers reported in PubMed according to the PRISMA guidelines. Individual miRNAs, mRNAs, lncRNAs and multigene panels, including the commercially available signatures, Oncotype DX and Prolaris, will be discussed; details related to cohort size, hazard ratio and 95% confidence intervals will be provided. Mechanistically, these individual biomarkers affect multiple pathways critical to tumorigenesis and progression, including epithelial-mesenchymal transition (EMT), phosphatase and tensin homolog (PTEN), Wnt, growth factor receptor, cell proliferation, immune checkpoints and others. This variety in the mechanisms involved not only validates their associations with BCR, but also highlights the need for the coverage of multiple pathways in order to effectively stratify the risk of BCR. Updates of novel biomarkers and their mechanistic insights are considered, which suggests new avenues to pursue in the prediction of BCR. Additionally, the management of patients with BCR and the potential utility of the stratification of the risk of BCR in salvage treatment decision making for these patients are briefly covered. Limitations will also be discussed. Contents 1. Introduction 2. Stratification of BCR risk: An update 3. Searching methods for RNA-based BCR biomarkers 4. Gene expression-based biomarkers 5. Management of patients with biochemical recurrence 6. Perspectives

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“…Numerous other lncRNAs in the GSE75970 dataset have not been characterized in terms of their roles in colon cancer. For example, PGM5-AS1 (NCBI, Gene, NR_015423) has been reported to regulate the miR-466/PTEN axis to exert tumor-suppressive effects in esophageal squamous cancer [22]; furthermore, abnormally low expression of PGM5-AS1 is related to the poor prognosis of renal clear cell carcinoma [23]. Zhu et al [24]downloaded the original microarray data set (GSE64857) containing analysis data of gene expression of patients suffering recurrent and non-recurrent CRC, and performed bioinformatics analysis to show that PGM5-AS1 was highly co-expressed with differentially expressed mRNAs.…”

Section: Resultsmentioning

confidence: 99%

PGM5-AS1 Inhibits the Malignant Phenotype of Colon Cancer Cells by Regulating PAEP and NME1

Hui

Chen

Wang

et al. 2020

Preprint

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Background: An increasing number of long non-coding RNAs (lncRNAs) is recognized to be associated with drug resistance in CRC.Methods: For identifying differentially expressed target genes regarding PGM5-AS1, RNA transcriptome sequencing was performed. The mechanism by which PGM5-AS1 regulates its target genes was explored by performing experiments such as fluorescent in situ hybridization assay, dual luciferase reporter gene assay and RNA immunoprecipitation. Results: The lncRNA PGM5-AS1 was identified by analyzing data from the original microarray data set of colon cancer (GSE75970). PGM5-AS1 additionally suppressed acquired oxaliplatin resistance in CRC cells. Malignant phenotype of PGM5-AS1 was inhibited by recruiting SRSF3 to activate alternative splicing and being a sponge specific to hsa-miR-423-5p.Conclusions: Downregulation of PGM5-AS1 in oxaliplatin-resistant colon cancer tissues and cell lines is induced by transcriptional inhibition of GFI1B. PGM5-AS1 recruited SRSF3 to activate alternative splicing to downregulate the expression of PAEP. In addition, PGM5-AS1 could competitively bind with hsa-miR-423-5p to upregulate the expression of NME1. PGM5-AS1 inhibits the proliferation, invasion, migration and acquired oxaliplatin resistance of colon cancer cells through these two pathways.

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p53‐induced long non‐coding RNA PGM5‐AS1 inhibits the progression of esophageal squamous cell carcinoma through regulating miR‐466/PTEN axis

Cited by 20 publications

References 37 publications

MiR-466 Inhibits the Progression of Severe Hepatocellular Carcinoma via Regulating FMNL2-Mediated Activation of NF-κB and Wnt/β-Catenin Pathways

MiR-466 Inhibits the Progression of Severe Hepatocellular Carcinoma via Regulating FMNL2-Mediated Activation of NF-κB and Wnt/β-Catenin Pathways

Assessment of biochemical recurrence of prostate cancer (Review)

PGM5-AS1 Inhibits the Malignant Phenotype of Colon Cancer Cells by Regulating PAEP and NME1

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