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 21 publications

(18 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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“…Esophageal squamous cell carcinoma (ESCC), which accounts for 90% of esophageal cancer, is the sixth leading cause of cancer-associated mortality, especially in several developing countries (1). Despite developments in medical and surgical treatment, the 5-year survival rate of ESCC is only 15-25%, largely because of recurrence of primary treatment and late stage diagnosis (2,3).…”

Section: Introductionmentioning

confidence: 99%

Mefloquine Inhibits Esophageal Squamous Cell Carcinoma Tumor Growth by Inducing Mitochondrial Autophagy

Xie

Zhang

et al. 2020

Front. Oncol.

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Esophageal squamous cell carcinoma (ESCC) has a worldwide impact on human health, due to its high incidence and mortality. Therefore, identifying compounds to increase patients' survival rate is urgently needed. Mefloquine (MQ) is an FDA-approved anti-malarial drug, which has been reported to inhibit cellular proliferation in several cancers. However, the anti-tumor activities of the drug have not yet been completely defined. In this study, mass spectrometry was employed to profile proteome changes in ESCC cells after MQ treatment. Sub-cellular localization and gene ontology term enrichment analysis suggested that MQ treatment mainly affect mitochondria. The KEGG pathway enrichment map of down-regulated pathways and Venn diagram indicated that all of the top five down regulated signaling pathways contain four key mitochondrial proteins (succinate dehydrogenase complex subunit C (SDHC), succinate dehydrogenase complex subunit D, mitochondrially encoded cytochrome c oxidase III and NADH: ubiquinone oxidoreductase subunit V3). Meanwhile, mitochondrial autophagy was observed in MQ-treated KYSE150 cells. More importantly, patient-derived xenograft mouse models of ESCC with SDHC high expression were more sensitive to MQ treatment than low SDHC-expressing xenografts. Taken together, mefloquine inhibits ESCC tumor growth by inducing mitochondrial autophagy and SDHC plays a vital role in MQ-induced anti-tumor effect on ESCC.

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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 21 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)

Mefloquine Inhibits Esophageal Squamous Cell Carcinoma Tumor Growth by Inducing Mitochondrial Autophagy

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