miR-193a-3p Promotes Radio-Resistance of Nasopharyngeal Cancer Cells by Targeting SRSF2 Gene and Hypoxia Signaling Pathway

Kong, Lingyun; Wei, Qing; Hu, Xianwen; Chen, Lanren; Li, Juan

doi:10.12659/msmbr.914572

Cited by 24 publications

(17 citation statements)

References 30 publications

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“…In 2012, Ma et al (2012) found that miR-193a-3p regulated the resistance of HCC to 5-FU via interacting with SRSF2 and E2F1, with SRSF2 being closely related to tumorigenicity of HCC cells and 5-FU resistance. Kong et al (2019) found that SRSF2 was negatively related to the expression level of miR-193a-3p in nasopharyngeal carcinoma via qRT-PCR. Mcl-1 ectopic expression reversed miR-193a-3p's promotion of apoptosis, and a reporter assay with a luciferase construct embracing a 3 -untranslated region of Mcl-1 verified that Mcl-1 is a direct target gene of miR-193a-3p (Kwon et al, 2013).…”

Section: Discussionmentioning

confidence: 96%

“…Recently, many researchers have verified that miR-193a-3p acts as an inhibitor in colon, gastric, and breast cancer because it suppressed the proliferation, migration, and invasion of these cancer cells (Chou et al, 2018;Pekow et al, 2017;Tsai et al, 2016). In addition, miR-193a-3p is involved in the tumorigenicity of nasopharyngeal carcinoma and HCC (Kong et al, 2019;Tsai et al, 2016). In 2015, our team also confirmed the low expression levels of miR-193a-3p in HCC tissues by means of qRT-PCR (Liu et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

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Downregulation of miR-193a-3p is involved in the pathogenesis of hepatocellular carcinoma by targeting CCND1

Wang

Huang

et al. 2020

PeerJ

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Background Hepatocellular carcinoma (HCC) is the second-highest cause of malignancy-related death worldwide, and many physiological and pathological processes, including cancer, are regulated by microRNAs (miRNAs). miR-193a-3p is an anti-oncogene that plays an important part in health and disease biology by interacting with specific targets and signals. Methods In vitro assays were performed to explore the influences of miR-193a-3p on the propagation and apoptosis of HCC cells. The sequencing data for HCC were obtained from The Cancer Genome Atlas (TCGA), and the expression levels of miR-193a-3p in HCC and non-HCC tissues were calculated. The differential expression of miR-193a-3p in HCC was presented as standardized mean difference (SMD) with 95% confidence intervals (CIs) in Stata SE. The impact of miR-193a-3p on the prognoses of HCC patients was determined by survival analysis. The potential targets of miR-193a-3p were then predicted using miRWalk 2.0 and subjected to enrichment analyses, including Gene Ontology (GO) annotation, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and Protein-Protein Interaction (PPI) network analysis. The interaction between miR-193a-3p and one predicted target, Cyclin D1 (CCND1), was verified by dual luciferase reporter assays and Pearson correlation analysis. Results MiR-193a-3p inhibited the propagation and facilitated the apoptosis of HCC cells in vitro. The pooled SMD indicated that miR-193a-3p had a low level of expression in HCC (SMD: −0.88, 95% CI [−2.36 −0.59]). Also, HCC patients with a higher level of miR-193a-3p expression tended to have a favorable overall survival (OS: HR = 0.7, 95% CI [0.43–1.13], P = 0.14). For the KEGG pathway analysis, the most related pathway was “proteoglycans in cancer”, while the most enriched GO term was “protein binding”. The dual luciferase reporter assays demonstrated the direct interaction between miR-193a-3p and CCND1, and the Pearson correlation analysis suggested that miR-193a-3p was negatively correlated with CCND1 in HCC tissues (R = − 0.154, P = 0.002). Conclusion miR-193a-3p could suppress proliferation and promote apoptosis by targeting CCND1 in HCC cells. Further, miR-193a-3p can be used as a promising biomarker for the diagnosis and treatment of HCC in the future.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Downregulation of miR-193a-3p is involved in the pathogenesis of hepatocellular carcinoma by targeting CCND1

Wang

Huang

et al. 2020

PeerJ

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“…Numerous targets of miR-193a-3p have been reported [26,28,32,33]. In this study, the TargetScan, miRNA.ORG, and miRDB software were used for the prediction of target genes.…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Mig-6 Promotes the Apoptosis and Inhibits of the Flux of Autophagy in HCC Cell Lines Through Modulating Mig-6/miR-193a-3p/TGF-β2 Axis

Tian

Hong

et al. 2020

Preprint

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Abstract Background:Mitogen-inducible gene 6 (Mig-6) is a tumor suppressor gene that plays an important role in many types of cancers by interacting with EGFR. Thus far, little is known about the molecular mechanism of Mig-6 in hepatocellular carcinoma (HCC). Also, the relationship between Mig-6 and miRNAs needs to be elucidated. Therefore, this study first aimed to find whether Mig-6 could promote apoptosis and inhibition of the flux of autophagy by its downstream miRNA in HCC cell lines. Methods: Two cell lines, HepG2and HLE, were used in this study. Mig-6 overexpression and knockdown models , miR-193a mimics and inhibitors models,were established. MiRNA microarray profiling were used to verified Mig-6 regulated- miRNA. Real-time PCR, Western blot analysis were carried out to detect RNA and protein expression.Evaluation of fluorescent LC3 puncta and cell fow cytometer assay were used to test the autophagy and apoptosis respectively. Results: Mig-6 induced the apoptosis and reduced the autophagy of HCC cell lines. MiR-193a-3p is a Mig-6-regulated miRNA in Mig-6 overexpression model, and miR-193a-3p affected the apoptosis and autophagy of HCC cells by regulating the expression of TGF-β2. Additionally, the relationship between Mig-6 and transforming growth factor TGF-β2 was explored in depth for the first time.Conclusion:These findings revealed an important regulatory axis Mig-6/miR-193a-3p/TGF-β2 in the apoptosis and autophagy of HCC cells, providing a novel insight into the therapeutic target in HCC.

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“…Moreover, they also explore dysregulated ncRNAs expression through comparing radiotherapy-resistant, radiotherapy-sensitive, and normal cancer tissues or cells, so as to discover key ncRNAs that could regulate radiotherapy sensitivity. We summarized the differently expressed ncRNAs in radiotherapy-resistant, radiotherapy-sensitive, and normal cancer tissues or cells as shown in Table 1 ( Qu et al, 2012 , 2015a , b ; Li et al, 2013 ; Li B. Y. et al, 2017 ; Li L. N. et al, 2017 ; Li et al, 2020 ; Shiiba et al, 2013 ; Zhang et al, 2013 ; Wang et al, 2014 , 2016 , Wang Z. et al, 2019 ; de Jong et al, 2015 ; Lin et al, 2015 ; Maia et al, 2015 ; Suh et al, 2015 ; Sun et al, 2015 ; Xu et al, 2015 ; Zhao et al, 2015 ; Huang et al, 2016 , 2018 , 2019 ; Kang et al, 2016 ; Weng et al, 2016 ; Wu et al, 2016 , 2018 ; Gao et al, 2017a , b ; Han et al, 2017 ; Hu et al, 2017 ; Chen H. et al, 2018 ; Chen et al, 2019 ; Feng et al, 2018 ; He et al, 2018 ; Yang et al, 2018 ; Kong et al, 2019 ; Tian et al, 2019 ; Vahabi et al, 2019 ; Yi et al, 2019 ; Gou et al, 2020 ; Kangboonruang et al, 2020 ; Shuai and Huang, 2020 ).…”

Section: Ionizing Radiation Modulates Ncrna Expression Profilingmentioning

confidence: 99%

Role of Non-coding RNAs on the Radiotherapy Sensitivity and Resistance of Head and Neck Cancer: From Basic Research to Clinical Application

Zhang

Yang

2021

Front. Cell Dev. Biol.

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Head and neck cancers (HNCs) rank as the sixth common and the seventh leading cause of cancer-related death worldwide, with an estimated incidence of 600,000 cases and 40–50% mortality rate every year. Radiotherapy is a common local therapeutic modality for HNC mainly through the function of ionizing radiation, with approximately 60% of patients treated with radiotherapy or chemoradiotherapy. Although radiotherapy is more advanced and widely used in clinical practice, the 5-year overall survival rates of locally advanced HNCs are still less than 40%. HNC cell resistance to radiotherapy remains one of the major challenges to improve the overall survival in HNC patients. Non-coding RNAs (ncRNAs) are newly discovered functional small RNA molecules that are different from messenger RNAs, which can be translated into a protein. Many previous studies have reported the dysregulation and function of ncRNAs in HNC. Importantly, researchers reported that several ncRNAs were also dysregulated in radiotherapy-sensitive or radiotherapy-resistant HNC tissues compared with the normal cancer tissues. They found that ectopically elevating or knocking down expression of some ncRNAs could significantly influence the response of HNC cancer cells to radiotherapy, indicating that ncRNAs could regulate the sensitivity of cancer cells to radiotherapy. The implying mechanism for ncRNAs in regulating radiotherapy sensitivity may be due to its roles on affecting DNA damage sensation, inducing cell cycle arrest, regulating DNA damage repair, modulating cell apoptosis, etc. Additionally, clinical studies reported that in situ ncRNA expression in HNC tissues may predict the response of radiotherapy, and circulating ncRNA from body liquid serves as minimally invasive therapy-responsive and prognostic biomarkers in HNC. In this review, we aimed to summarize the current function and mechanism of ncRNAs in regulating the sensitivity of HNC cancer cells to radiotherapy and comprehensively described the state of the art on the role of ncRNAs in the prognosis prediction, therapy monitoring, and prediction of response to radiotherapy in HNC.

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miR-193a-3p Promotes Radio-Resistance of Nasopharyngeal Cancer Cells by Targeting SRSF2 Gene and Hypoxia Signaling Pathway

Cited by 24 publications

References 30 publications

Downregulation of miR-193a-3p is involved in the pathogenesis of hepatocellular carcinoma by targeting CCND1

Downregulation of miR-193a-3p is involved in the pathogenesis of hepatocellular carcinoma by targeting CCND1

WITHDRAWN: Mig-6 Promotes the Apoptosis and Inhibits of the Flux of Autophagy in HCC Cell Lines Through Modulating Mig-6/miR-193a-3p/TGF-β2 Axis

Role of Non-coding RNAs on the Radiotherapy Sensitivity and Resistance of Head and Neck Cancer: From Basic Research to Clinical Application

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