Attenuation of deregulated miR-369-3p expression sensitizes non-small cell lung cancer cells to cisplatin via modulation of the nucleotide sugar transporter SLC35F5

Hao, Guangjun; Wen, H. Joseph; Li, Xiaofeng; Zhang, Wei; Su, Hu-yan; Liu, Dongmei; Xie, Nianlin

doi:10.1016/j.bbrc.2017.05.075

Cited by 28 publications

(18 citation statements)

References 16 publications

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“…Several studies have reported that some miRNAs, such as miR-200c [33] and miR-23a [30], can be used as potential therapeutic approaches to EEC. Furthermore, expression levels of miRNA-200c significantly increased in endometrioid endometrial cancer samples.…”

Section: Discussionmentioning

confidence: 99%

MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy

Liu

et al. 2019

Cancer Cell Int

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Background The aim of this study is to examine miRNA profiling and miR-369-3p participates in endometrioid adenocarcinoma (EEC) via the regulation of autophagy. Methods EEC and its adjacent normal tissues were obtained from 20 clinical patients after surgery. MiRNA profiling was performed using next generation sequencing (NGS) and was validated with quantitative real time PCR (qRT-PCR). qRT-PCR was also employed to measure miR-369-3p and autophagy-related protein 10 (ATG10) expression levels. Western blotting assay was performed to measure the expressions of ATG10 and LC3B. Luciferase reporter assay was conducted to confirm the direct targeting of ATG10 by miR-369-3p. Cell proliferation and migration assays were utilized to analyze the role of miR-369-3p in HEC-1-A cells. Results We found that miR-369-3p expression levels were down-regulated in EEC compared to the control tissues. The overexpression of miR-369-3p inhibited cell proliferation and migration in EEC; furthermore, ATG10 expression increased in EEC tissues. ATG10 was found to be a potential target of miR-369-3p via a dual-luciferase reporter assay, and ATG10 was shown to be down-regulated by miR-369-3p in protein levels. Conclusions This study revealed that miR-369-3p inhibited cell proliferation and migration by targeting ATG10 via autophagy in EEC. Electronic supplementary material The online version of this article (10.1186/s12935-019-0897-8) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy

Liu

et al. 2019

Cancer Cell Int

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“…A to the normal tissues. In the same study, the inhibition of miR-369-3p sensitized lung cancer cells to DDP and attenuated their invasion capability by targeting human solute carrier 35F5 (SLC35F5) [18]. Pan et al [31] found that in Hirschsprung disease (HSCR) tissues miR-369-3p was significantly upregulated compared to adjacent normal tissues.…”

Section: E C Bmentioning

confidence: 95%

“…For instance, the expression of miR-369-3p was increased in serum samples and skin tissues of psoriasis patients, and was in positive correlation with disease severity [17]. In cisplatin (DDP)-resistant nonsmall cell lung cancer (NSCLC) tissues, the inhibition of miR-369-3p induced sensitivity of NSCLC cells to and suppressed their invasive capability in the presence of DDP, and conversely, the overexpression of miR-369-3p promoted resistance of NSCLC to DDP and enhanced their invasiveness [18]. However, the role of miR-369-3p in thyroid cancer is still not clear.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of TSPAN13 by miR-369-3p inhibits cell proliferation in papillary thyroid cancer (PTC)

Dong

Wang

2018

Bosn J of Basic Med Sci

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Previous studies demonstrated dysregulation of different microRNAs in thyroid cancer. Tetraspanins (TSPANs) are cell surface proteins with critical roles in many cellular processes, and implications in tumor development. Here we investigated the role of miR-369-3p in papillary thyroid cancer (PTC) and its association with TSPAN13. miR-369-3p and the TSPAN13 gene expression profiles of 513 thyroid cancer and 59 normal thyroid tissues were downloaded from the Cancer Genome Atlas database. Thyroid cancer tissues were classified according to the histological type, grouped based on low and high median miR-369-3p and TSPAN13 expression, and analyzed in relation to overall survival (OS) of patients. Human PTC cell lines (TPC-1 and GLAG-66) and human embryonic kidney 293T (HEK293T) cells were used for in vitro analysis. Transfection experiments were performed with synthetic miRNA mimics for miR-369-3p and small interfering RNAs for TSPAN13. Relative expression of miR-369-3p and TSPAN13 mRNA was determined by RT-qPCR. Protein levels of TSPAN13 were determined by western blotting. Cell proliferation (CCK-8 assay), colony formation, and apoptosis (flow cytometry) were analyzed in transfected cells. Binding sites of miR-369-3p in TSPAN13 mRNA were determined by bioinformatics analysis and dual luciferase reporter assay. miR-369-3p was downregulated and TSPAN13 upregulated in PTC, follicular thyroid cancer, and tall cell variant tissues. Both low expression of miR-369-3p and high expression of TSPAN13 were associated with shorter OS in thyroid cancer patients. Overexpression of miR-369-3p significantly suppressed proliferation and promoted apoptosis in PTC cells. TSPAN13 was a direct target of miR-369-3p, and silencing of TSPAN13 phenocopied the effect of miR-369-3p mimics in PTC cells. Overall, the downregulation of miR-369-3p and consequent upregulation of its target TSPAN13 appear to be involved in pathophysiology of PTC.

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“…Moreover, the downregulated miR-144-3p was correlated to poor diseasefree survival. As for miR-369-3p and miR-374b-5p, they were dysregulated in various types of cancers, but no study has been conducted to explore their functions and mechanisms in HCC [56][57][58][59][60].…”

Section: Discussionmentioning

confidence: 99%

Clinical Value and Potential Mechanisms Exploration of GOLGA8B in Hepatocellular Carcinoma: A Comprehensive Investigation Based on Real-Time Quantitative Polymerase Chain Reaction, RNA-seq, Microarray and Immunohistochemistry

Ma¹,

Zhai²,

Wu³

et al. 2019

Preprint

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Introduction Recent studies found that GOLGA8B plays an essential role in different cancers. However, the role GOLGA8B plays in the carcinogenesis and development of hepatocellular carcinoma (HCC) remains unclear. This study explores the clinical significance and prospective mechanisms of GOLGA8B in HCC. Materials and methods The expression of GOLGA8B was detected in tissues of HCC and non-HCC controls. A real-time quantitative polymerase chain reaction analysis was performed to evaluate the mRNA expression of GOLGA8B. RNA-sequencing data and microarray chip data were obtained for further analysis. The role GOLGA8B plays in patients with HCC was also evaluated. An immunohistochemistry (IHC) analysis was also performed to evaluate the protein expression of GOLGA8B. The different GOLGA8B expression resources, including mRNA and protein expression, were integrated by calculating standard mean difference (SMD) and summary of the receiver operator characteristic (sROC). Genes co-expressed GOLGA8B were predicted. Enrichment analyses including Gene ontology (GO) and biological pathway were performed to investigate the essential molecular mechanisms. Hub genes were screened out by a protein-protein interactions network. MicroRNAs which target GOLGA8B at a posttranscriptional level were also predicted. Results According to different resources, GOLGA8B manifested a higher expression in tissues of HCC than in non-HCC controls and exhibited clinical values for HCC. The RT-qPCR analysis revealed an increasing trend of GOLGA8B expression in HCC. GOLGA8B expresssion was significantly increased in RNA-sequencing and 7 of 13 microarray chip. IHC analysis also revealed significantly higher expression of GOLGA8B protein. Moreover, GOLGA8B expression was correlated with pathologic tumors and stages according to RNA-sequencing data and IHC analysis. The integrated SMD and sROC of different resources was 0.893 (P=0.004) and 0.79. A total 1303 co-expressed genes were gathered to perform enrichment analyses. The most significant biological pathways of co-expressed genes were spliceosome and mitogen-activated protein kinase signalling (MAPK). Four hub genes (SF3B1, HNRNPA2B1, HNRNPA1 and SRRM2) and five miRNAs (miR-369-3p, miR-203a, miR-374b-5p, miR-139-5p and miR-144-3p) were screened out. Conclusion GOLGA8B expression was increased in HCC and may serve as a novel target for HCC diagnosis and treatment.

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Attenuation of deregulated miR-369-3p expression sensitizes non-small cell lung cancer cells to cisplatin via modulation of the nucleotide sugar transporter SLC35F5

Cited by 28 publications

References 16 publications

MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy

MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy

Downregulation of TSPAN13 by miR-369-3p inhibits cell proliferation in papillary thyroid cancer (PTC)

Clinical Value and Potential Mechanisms Exploration of GOLGA8B in Hepatocellular Carcinoma: A Comprehensive Investigation Based on Real-Time Quantitative Polymerase Chain Reaction, RNA-seq, Microarray and Immunohistochemistry

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