The long non-coding RNA MIAT/miR-139-5p/MMP2 axis regulates cell migration and invasion in non-small-cell lung cancer

et al. 2018

OTT

PurposeFocusing on the latest literature, dysregulated long non-coding RNAs (lncRNAs) have been extensively explored in breast cancer (BC) research. The purpose of this meta-analysis is to synthesize the evidence on the diagnostic performance of abnormally expressed lncRNAs for BC.Materials and methodsRelevant studies were searched in multiple electronic databases. The Quality Assessment of Diagnosis Accuracy Studies II criteria were applied to assess the quality of included studies. The bivariate meta-analysis model was applied to synthesize the diagnostic parameters using Stata 12.0 software. Publication bias was judged in terms of the Deek’s funnel plot asymmetry test.ResultsWe included 10 eligible studies, which comprised 835 BC patients and 725 paired controls for this meta-analysis. The pooled sensitivity, specificity, diagnostic odds ratio, likelihood ratio positive, likelihood ratio negative, and area under the curve (AUC) of upregulated lncRNA expression signature in confirming BC were 0.79 (95% CI: 0.70–0.85), 0.80 (95% CI: 0.73–0.85), 14.61 (95% CI: 10.91–19.55), 3.90 (95% CI: 3.03–5.02), 0.27 (95% CI: 0.20–0.36), and 0.86, respectively. Stratified analyses yielded a sensitivity of 0.83 (95% CI: 0.80–0.86) for serum-based analysis, which was higher than plasma-based analysis, whereas plasma-based analysis revealed a greater specificity of 0.88 (95% CI: 0.85–0.91). Moreover, lncRNA-homeotic genes (HOX) transcript antisense RNA showed a pooled specificity of 0.89 (95% CI: 0.84–0.93) and AUC of 0.86, which were superior to performances by lncRNA-metastasis-associated lung adenocarcinoma transcript-1 and -H19 in diagnosing BC. Notably, the analysis based on cancer subtypes demonstrated that lncRNA expression signature could distinguish triple-negative BC (lacks estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 expression) from non-triple-negative BC, with an AUC of 0.85.ConclusionUpregulated lncRNAs reveal an immense potential as novel non-invasive biomarker(s) that could complement BC diagnosis.

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Upregulated long non-coding RNAs demonstrate promising efficacy for breast cancer detection: a meta-analysis

Gao

Zhang²,

et al. 2018

OTT

CircTHBS1 facilitates the progression of interstitial cystitis depending on the regulation of miR‐139‐5p/MFN2 axis

Jiang

Drug Development Research

et al. 2021

Circular RNA (circRNA) have been found to play an important role in the progression of many diseases, including interstitial cystitis (IC). However, the role of circTHBS1 in IC progression is still unclear. Exploring the role and potential molecular mechanism of circTHBS1 in the development of IC. The enzyme‐linked immunosorbent assay was used to assess the levels of inflammatory cytokines. The expression levels of circTHBS1, microRNA (miR)‐139‐5p, and mitofusin 2 (MFN2) were evaluated using quantitative real‐time PCR. Cell proliferation and migration were determined using MTT assay, Edu staining, and transwell assay. The protein levels of epithelial‐mesenchymal transition (EMT) markers and MFN2 were examined using western blot analysis. The relationship between miR‐139‐5p and circTHBS1 or MFN2 was confirmed using the dual‐luciferase reporter assay and RIP assay. CircTHBS1 was highly repressed in IC tissues and cells, and its expression was positively correlated with the inflammatory response of IC patients. CircTHBS1 could promote the proliferation, migration, EMT process, and inflammation of IC cells, while its knockdown had an opposite effect. CircTHBS1 could serve as a sponge of miR‐139‐5p, and miR‐139‐5p could participate in the regulation of circTHBS1 on IC cell progression. In addition, miR‐139‐5p could target MFN2, and it could inhibit the progression of IC cells by targeting MFN2. Furthermore, circTHBS1 sponged miR‐139‐5p to positively regulate MFN2. CircTHBS1 promoted IC cell proliferation, migration, EMT process, and inflammation by regulating the miR‐139‐5p/MFN2 axis indicating that circTHBS1 might be a potential target for IC treatment.

circ_0008797 attenuates non‐small cell lung cancer proliferation, metastasis, and aerobic glycolysis by sponging miR‐301a‐3p/SOCS2

Abuduwaili

Environmental Toxicology

Shen

et al. 2022

Purpose: This paper firstly reported the exact function of circ_0008797 on non-small cell lung cancer (NSCLC) progression.Methods: NSCLC tissues/matched normal tissues were harvested from 88 NSCLC patients. RNA fluorescence in situ hybridization experiment was applied to detect circ_0008797 localization in NSCLC cells. circ_0008797 effect on NSCLC cells proliferation, migration, invasion, glucolysis, and apoptosis was researched by cell counting kit-8 assay, 5-ethynyl-2'deoxyuridine assay, Transwell experiment, glycolysis assay, and TUNEL assay. Dual luciferase reporter gene assay, RNA pull-down assay and RNA immunoprecipitation assay were used to verify the binding relationship between two genes. In vivo tumorigenesis and lung metastasis was performed using nude mice. Quantitative reverse transcription-polymerase chain reaction, immunohistochemistry and western blot were applied for genes expression detection. Hematoxylin and eosin staining was performed on lung tissues.Results: circ_0008797 was low expressed in NSCLC tissues and cell lines, associating with poor outcome (p <.05). circ_0008797 was mainly expressed in NSCLC cells cytoplasm. circ_0008797 inhibited proliferation, migration, invasion, and glycolysis, but enhanced apoptosis of NSCLC cells (p <.05). circ_0008797 attenuated malignant phenotype of NSCLC cells by sponging miR-301a-3p. circ_0008797 facilitated SOCS2 expression by sponging miR-301a-3p. SOCS2 knockdown partially reversed the inhibitory effect of miR-301a-3p inhibition on NSCLC cells malignant phenotype (p <.05). circ_0008797 attenuated NSCLC prolifearion and metastasis in vivo (p <.05). Conclusion: circ_0008797 attenuates NSCLC proliferation, metastasis and aerobicglycolysis by sponging miR-301a-3p/SOCS2.