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Background: Long non-coding RNA (lncRNA) is implicated in the progression of multiple cancers. This study aimed to explore the expression characteristics, biological function and molecular mechanism of lncRNA HAGLROS expression in NSCLC., Methods: Quantitative real-time polymerase chain reaction (RT-PCR) was adopted to detect HAGLROS expression in NSCLC tissues and normal lung tissues. Survival curve was plotted by Kaplan-Meier method. Gain-of-function and loss-of-function models were respectively established to investigate the biological functions of HAGLROS, miR-100 and SMARCA5. MTT and Transwell assays were carried out to monitor the changes in proliferation, migration and invasion of NSCLC cells. Bioinformatics analysis and dual-luciferase reporter assay were used to verify the binding sites between HAGLROS and miR-100. Western blot was performed to determine the regulatory effects of HAGLROS and miR-100 on SMARCA5 protein expression., Results: Up-regulated HAGLROS expression was observed in NSCLC tissues and cell lines. Over-expressed HAGLROS promoted the malignant phenotypes of NSCLC cells; conversely, HAGLROS knockdown repressed the malignant phenotypes of NSCLC cells. HAGLROS repressed miR-100 expression to promote SMARCA5 expression in NSCLC cells, and miR-100 overexpression or SMARCA5 knockdown counteracted the oncogenic functions of HAGLROS., Conclusions: These results conclude that HAGLROS is a tumor promoter in NSCLC, and it regulates the malignant phenotypes of NSCLC cells via miR-100/SMARCA5 axis., Competing Interests: Conflicts of interest The authors declare that they have no competing interest., (Copyright © 2022 Chang Gung University. Published by Elsevier B.V. All rights reserved.)

Gastric cancer (GC) is a common malignant digestive tract tumor that leads to high mortality worldwide. Early diagnosis of GC is very important for adequate treatment. However, a rapid, specific and sensitive method for the detection of GC is currently not available. Here, a biosensor CPs/AuNP-AuE, the gold nanoparticle (AuNP)-modified Au electrode (AuE) which was coupled with DNA capture probes (CPs), was developed to detect the content of miR-100 in the sera of GC patients. The results showed that AuNPs were uniformly deposited on the surface of AuE. AuNPs enhanced the electrical conductivity and improved the effective area of AuE. CPs were successfully assembled on AuNP-AuE that could be digested by duplex-specific nuclease (DSN) from the miR-100/CPs complex on the electrode, improving the sensitivity of the biosensor by recycling miR-100. The data revealed that the biosensor was highly specific for the detection of miR-100, which had the ability to distinguish one base-pair mistake in miR-100. The detection of the biosensor for miR-100 ranged from 100 aM to 10 pM and the limit of detection (LOD) was estimated to be 100 aM. The detection results of 100 human sera samples using this biosensor indicated that the cutoff for the detection of gastric cancer was 5 fM. Therefore the biosensor developed in our study served as a rapid, specific and sensitive strategy for the detection of gastric cancer in clinic., (Copyright © 2020. Published by Elsevier B.V.)

Purpose: Overexpression of miR-100 in stem cells derived from basal-like breast cancers causes loss of stemness, induction of luminal breast cancer markers and response to endocrine therapy. We, therefore, explored miR-100 as a novel biomarker in patients with luminal breast cancer., Methods: miR-100 expression was studied in 90 patients with oestrogen-receptor-positive/human-epidermal growth factor receptor 2-negative breast cancer enrolled in a prospective study of endocrine therapy given either preoperatively, or for the treatment of de novo metastatic disease. Response was defined as a Ki67 ≤2.7% after 21±3 days of treatment. The prognostic role of miR-100 expression was evaluated in the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) and The Cancer Genome Atlas (TCGA) breast cancer datasets. Additionally, we explored the correlation between miR-100 and the expression its targets reported as being associated with endocrine resistance. Finally, we evaluated whether a signature based on miR-100 and its target genes could predict the luminal A molecular subtype., Results: Baseline miR-100 was significantly anticorrelated with baseline and post-treatment Ki67 (p<0.001 and 0.004, respectively), and independently associated with response to treatment (OR 3.329, p=0.047). In the METABRIC dataset, high expression of miR-100 identified women with luminal A tumours treated with adjuvant endocrine therapy with improved overall survival (HR 0.55, p<0.001). miR-100 was negatively correlated with PLK1, FOXA1, mTOR and IGF1R expression, potentially explaining its prognostic effect. Finally, a miR-100-based signature developed in patients enrolled in the prospective study outperformed Ki67 alone in predicting the luminal A phenotype., Conclusions: Our findings suggest that miR-100 should be further explored as a biomarker in patients with luminal breast cancer., Competing Interests: Competing interests: FM has received personal speaker’s fees from Roche, Novartis, Pfizer, Pierre Fabre, Eli Lilly, Daiichi Sankyo, Astra Zeneca. EB is the recipient of a Ph.D. fellowship from the Department of Medical Sciences, University of Torino ('Dipartimenti di Eccellenza 2018–2022', Project no. D15D18000410001)., (© Author (s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. Published by BMJ on behalf of the European Society for Medical Oncology.)

Acute myeloid leukemia (AML) is the most common pediatric malignancy and a major cause of morbidity and mortality in children. miR-100 is associated with progression of various diseases including AML. The aim of this study was to explore the underlying molecule mechanisms of miR-100 involved in AML. The expressions of miR-100 and ataxia telangiectasia mutated (ATM) in pediatric AML patients and cell lines were monitored using qRT-PCR and western blot assays. MTT assay was carried to evaluate cell viability. Cell apoptosis was measured by flow cytometry. The binding sites between miR-100 and ATM were predicted by mirtarbase database. Luciferase reporter assay was used to confirm the relationship between miR-100 and ATM. miR-100 expression was highly expressed in bone marrow of AML patients and cell lines. Moreover, Knockdown of miR-100 led to the inhibition of viability and promotion of apoptosis in Kasumi-1 and MV-4-11 cells. miR-100 harbored the 3'UTR of ATM. Meanwhile, the expression of ATM was downregulated in bone marrow of AML patients and AML cell lines. Subsequently, a negative correlation between miR-100 and ATM in bone marrow of AML patients was also observed. Furthermore, ectopic expression of ATM repressed cell viability while enhanced apoptosis. Notably, loss of ATM attenuated the effect of miR-100 depletion on cell viability and apoptosis in AML cells. miR-100 participates in cell viability and apoptosis by targeting ATM in pediatric AML., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interests., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Pneumonia is a lower respiratory disease caused by pathogens or other factors. This study aimed to explore the roles and mechanism of long noncoding RNA HAGLROS in lipopolysaccharides (LPS)-induced inflammatory injury in pneumonia. The HAGLROS expression in serum of patients with acute stage pneumonia was detected. To induce pulmonary injury, WI-38 human lung fibroblasts were stimulated with lipopolysaccharides (LPS). The HAGLROS expressions in LPS-treated WI-38 cells and the effects of HAGLROS knockdown on the viability, apoptosis, and autophagy of LPS-induced cells were detected. Moreover, the regulatory relationship between HAGLROS and miR-100 was explored as well as the functional targets of miR-100 were identified. Furthermore, the regulatory relationship between miR-100 and PI3K/AKT/NF-κB pathway was elucidated. LncRNA HAGLROS was higher expressed in serum of patients with acute stage pneumonia compared with that in serum of healthy control. LPS caused WI-38 cell injury and increased HAGLROS levels. Downregulation of HAGLROS alleviated LPS-induced cell injury via increasing cell viability, and inhibiting apoptosis and autophagy. Moreover, there was a negative correlation between HAGLROS and miR-100, and the effects of HAGLROS downregulation on LPS-induced apoptosis and autophagy in WI-38 cells were by regulation of miR-100. Furthermore, NFΚB3 was verified as a functional target of miR-100 and effects of miR-100 inhibition on LPS-induced WI-38 cell injury were alleviated by knockdown of NFΚB3. Besides, Knockdown of HAGLROS inhibited the activation of PI3K/AKT/NF-κB pathway. Our findings reveal that downregulation of HAGLROS may alleviate LPS-induced inflammatory injury in WI-38 cells via modulating miR-100/NF-κB axis. HAGLROS/miR-100/NF-κB axis may provide a new strategy for treating acute stage of pneumonia., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

In most insect species, the microRNA (miRNA) let-7 clusters with miR-100 and miR-125 in the same primary transcript. The three miRNAs are involved in developmental timing in the nematode Caenorhabditis elegans and in the fly Drosophila melanogaster. In the cockroach Blattella germanica, the expression of these miRNAs increases dramatically in the wing pads around the molting peak of 20-hydroxyecdysone (20E) of the last instar nymph. When let-7 and miR-100 were depleted with specific anti-miRNAs in this instar, the resulting adults showed wings reduced in size (when miR-100 was depleted) or with malformed vein patterning (when let-7 and miR-100 were depleted). Depletion of miR-125 induced no apparent effects. Interestingly, the wing phenotype obtained after depleting let-7 and miR-100 is similar to that resulting from silencing the expression of Broad-Complex (BR-C) transcription factors with RNA interference (hindwings with a short CuP vein, with the vein/inter-vein pattern disorganized in the anterior part and showing anomalous bifurcations of the A-veins in the posterior part)., (Copyright © 2013 Elsevier Ltd. All rights reserved.)