Crosstalk between the Notch signaling pathway and non‑coding RNAs in gastrointestinal cancers (Review)

Mao, Yuliang; Jin, Rong; Jiang, Lei

doi:10.3892/ol.2017.7294

Cited by 8 publications

(8 citation statements)

References 100 publications

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“…LncRNAs affect angiogenesis by regulating various angiogenetic molecules, endothelial cell behaviors and tube formation. Besides, a cascade of lncRNAs have been found to participate in the angiogenesis-related pathways, such as vascular endothelial growth factor (VEGF) [ 21 , 22 ] and Notch [ 23 ]. Therefore, angiogenesis-related lncRNAs (ARlncR) as a kind of potential candidate, merit further discovery and attention in the field of antiangiogenetic strategies.…”

Section: Introductionmentioning

confidence: 99%

A novel risk score model based on five angiogenesis-related long non-coding RNAs for bladder urothelial carcinoma

Zhang

Peng

et al. 2022

Cancer Cell Int

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Background Tumour angiogenesis is an independent risk factor for bladder urothelial carcinoma (BUC) progression, but viable and promising antiangiogenic targets are understudied. Emerging evidence suggests that long non-coding RNAs (lncRNAs) play prominent role in the tumour microenvironment and tumour angiogenesis. Methods The clinical data of BUC patients were obtained from TCGA database and clinical specimens of 138 BUC patients. Univariate and multivariate COX regression analyses were used to identify survival-related ARLNRs (sARLNRs) from The Molecular Signatures Database v4.0. Fisher’s exact probability method was used to detect the correlations between sARLNRs levels and clinicopathological characteristics. A chain of experiments including FACS, qPCR, immunohistochemistry, tube formation, migration and invasion assays, combining with co-culture models, were utilized to validate the clinical significance and angiogenetic correlation of sARLNRs. Results Five sARLNRs were employed to establish an angiogenesis-related risk score model, by which patients in the low-risk group obtained better overall survival than those in the high-risk group. The expression of AC005625.1 and AC008760.1 was significantly related to ECs percentage, tumour size and muscle invasion status. Besides, AC005625.1 and AC008760.1 expressed lower in BUC cell lines and tumour tissues than that in normal urothelial cells and adjacent normal tissues, with much lower levels in more advanced T stages. A prominently higher proportion of ECs was detected in tumour tissues with lower expression of AC005625.1 and AC008760.1. In the co-culture models, we found that knockdown of AC005625.1 and AC008760.1 in BUC cells increased the tube formation, migration and invasion abilities of HUVEC. The expression levels of CD31, VEGF-A, VIMENTIN and N-CADHERIN were also enhanced in HUVEC cells co-cultured with siR-AC005625.1 and siR-AC008760.1-treated T24 cells. Conclusion In the study, we identify five sARLNRs and validate their clinical significance, angiogenesis correlation and prognosis-predictive values in BUC. These findings may provide a new perspective and some promising antiangiogenic targets for clinical diagnosis and treatment strategies of BUC.

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Section: Introductionmentioning

confidence: 99%

A novel risk score model based on five angiogenesis-related long non-coding RNAs for bladder urothelial carcinoma

Zhang

Peng

et al. 2022

Cancer Cell Int

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show abstract

“…LncRNAs affect angiogenesis by regulating various angiogenetic molecules, endothelial cell behaviors and tube formation. Besides, a cascade of lncRNAs have been found to participate in the angiogenesis-related pathways, such as vascular endothelial growth factor (VEGF) 21,22 and Notch 23 . Therefore, angiogenesis-related lncRNAs (ARlncR) as a kind of potential candidate, merit further discovery and attention in the eld of antiangiogenetic strategies.…”

Section: Introductionmentioning

confidence: 99%

A novel risk score model based on five angiogenesis-related long non-coding RNAs for bladder urothelial carcinoma

Zhang

Xiang

et al. 2022

Preprint

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Background Tumour angiogenesis is an independent risk factor for bladder urothelial carcinoma (BUC) progression, but viable and promising antiangiogenic targets are understudied. Long non-coding RNAs (lncRNAs) have been reported to play significant roles in angiogenesis. Methods The clinical data of BUC patients were obtained from TCGA database and clinical specimens of 138 BUC patients. Angiogenesis-related long non-coding RNAs (ARLNRs) were extracted from The Molecular Signatures Database v4.0. Univariate and multivariate COX regression analyses were used to further identify survival-related ARLNRs (sARLNRs). A chain of techniques (FACS, western blotting, qPCR, immunohistochemistry, tube formation, migration and invasion assays) and co-culture models were utilized to validate the clinical significances and angiogenetic correlation of sARLNRs. Results Five sARLNRs were employed to establish angiogenesis-related risk score model, by which the patients in the low-risk group obtained longer overall survival than those in the high-risk group. Two sARLNRa in the risk score model (AC005625.1 and AC008760.1) expressed lower in BUC cell lines and tumour tissues than that in normal urothelial cells and adjacent normal tissues, with further lower expression in more advanced T stages. More importantly, the expression of AC005625.1 and AC008760.1 expression was negatively related to endothelial cells (ECs) percentage, tumour size and muscle invasion status. A prominently higher proportion of ECs was detected in tumour tissues with lower expression of AC005625.1 and AC008760.1. Furthermore, in the co-culture model of T24 cells and HUVEC cells, knockdown of AC005625.1 and AC008760.1 in BUC cells increased tube formation, migration and invasion abilities of HUVEC cells. The expression levels of CD31, VEGF-A, VIMENTIN and N-CADHERIN were also enhanced in HUVEC cells co-cultured with siR-AC005625.1 and siR-AC008760.1-treated T24 cells. Conclusion In the study, we identify five sARLNRs and validate their clinical significances, angiogenesis correlation and prognosis-predictive values in BUC. These results may provide a new perspective and some promising antiangiogenic targets for clinical diagnosis and treatment strategies of BUC.

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“…Long non‐coding RNAs (lncRNAs) are a new type of RNA molecules of 200–200,000 nucleotides in length that do not encode proteins, and they can participate in the regulation of gene expression by affecting transcriptional regulation, post‐transcriptional regulation and chromatin modification gene imprinting 4–7 . lncRNAs are involved in the regulation of differentiation, apoptosis and cell cycles of a variety of cancers 8 .…”

Section: Introductionmentioning

confidence: 99%

Inhibition of lncRNA DCST1‐AS1 suppresses proliferation, migration and invasion of cervical cancer cells by increasing miR‐874‐3p expression

Zhang¹,

Hu²,

Zou³

et al. 2020

The Journal of Gene Medicine

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BackgroundCervical cancer seriously threatens both the health and life of women. We aimed to investigate whether RNA interference of long non‐coding RNA (lncRNA) DCST1‐AS1 could promote miR‐874‐3p expression to affect the proliferation, migration and invasion of cervical cancer cells.MethodsDCST1‐AS1 expression levels in cervical cancer cells and transfection effects were detected by quantitative reverse transcriptase‐polymerase chain reaction analysis. Proliferation, invasion and migration of cells were separately shown by cell‐counting kit‐8, wound healing and transwell assays, and relative protein expression was determined by western blot analysis. Dual‐luciferase reporter and RNA immunoprecipitation assays verified the interaction of DCST1‐AS1 and miR‐874‐3p.ResultsDCST1‐AS1 expression was increased in cervical cancer tissues and cells. The DCST1‐AS1 expression in Hela and SiHa cells was the highest, and so the cells were selected for the next experiment. Inhibition of DCST1‐AS1 suppressed the proliferation, invasion and migration of cervical cancer cells and decreased the expression of KI67, proliferating cell nuclear antigen, matrix metalloproteinase (MMP)‐2 and MMP‐9. miR‐874‐3p expression was increased when cells were transfected with miR‐874‐3p mimic or shRNA‐DCST1‐AS1‐1, and DCST1‐AS1 expression was down‐regulated when cells were transfected with miR‐874‐3p mimic. DCST1‐AS1 can directly target miR‐874‐3p. Furthermore, inhibition of miR‐874‐3p could effectively alleviate the effect of inhibition of DCST1‐AS1 with respect to the proliferation, invasion and migration of cervical cancer cells.ConclusionsInhibition of DCST1‐AS1 suppressed the proliferation, migration and invasion of cervical cancer cells by increasing miR‐874‐3p expression, which could be alleviated by the inhibition of miR‐874‐3p.

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Crosstalk between the Notch signaling pathway and non‑coding RNAs in gastrointestinal cancers (Review)

Cited by 8 publications

References 100 publications

A novel risk score model based on five angiogenesis-related long non-coding RNAs for bladder urothelial carcinoma

A novel risk score model based on five angiogenesis-related long non-coding RNAs for bladder urothelial carcinoma

A novel risk score model based on five angiogenesis-related long non-coding RNAs for bladder urothelial carcinoma

Inhibition of lncRNA DCST1‐AS1 suppresses proliferation, migration and invasion of cervical cancer cells by increasing miR‐874‐3p expression

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