Long non-coding RNA NEAT1 promotes colorectal cancer progression by competitively binding miR-34a with SIRT1 and enhancing the Wnt/β-catenin signaling pathway

Luo, Yang; Chen, Jianjun; Lv, Qiang; Qin, Jun; Huang, Yizhou; Yu, Minhao; Zhong, Ming

doi:10.1016/j.canlet.2018.10.002

Cited by 117 publications

(102 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…proliferation and invasion of CRC cells and function as ceRNAs to modulate miRNA-34a expression, subsequently causing the repression of the miR-34a/SIRT1 axis [23,24]. The lncRNA plasmacytoma variant translocation 1 (PVT1)-214 acts as an oncogene that can facilitate proliferation, migration, and invasion in CRC cells by reducing Lin28 protein degradation and enhancing its stability and by increasing Lin28 at the posttranscriptional level by binding to miR-128 [25].…”

Section: Discussionmentioning

confidence: 99%

The novel long noncoding RNA CRART16 confers cetuximab resistance in colorectal cancer cells by enhancing ERBB3 expression via miR-371a-5p

et al. 2020

View full text Add to dashboard Cite

Background: Long noncoding RNAs (lncRNAs) have been shown to participate in multiple biological processes and confer drug resistance. However, it remains unclear whether lncRNAs are involved in conferring cetuximab resistance in colorectal cancer (CRC) cells.Methods: Cell Counting Kit-8 (CCK-8) assays were performed to assess the sensitivity of CRC cell lines to cetuximab treatment. -2 cells were stably transduced with cetuximab resistance-associated RNA transcript 16 (CRART16) or an empty vector using lentiviral infection; the cells were designated Caco-2-CRART16 and Caco-2-NC, respectively, and were analyzed with RNA sequencing (RNA-seq). Quantitative real-time PCR (qRT-PCR) was performed to investigate RNA expression. Flow cytometry and TUNEL assays were used to assess apoptosis levels induced by cetuximab. The cell cycle, stemness biomarkers and membrane proteins of CRC cells were assessed via flow cytometry. RNA fluorescence in situ hybridization (FISH) was used to examine CRART16 localization and expression. Bioinformatics analysis was performed to predict the potential mechanism of CRART16, which was further validated by a dual-luciferase reporter assay. Differences in measurement data were compared using Student's t test, one-way ANOVA followed by Dunnett's test and two-way ANOVA.

show abstract

Section: Discussionmentioning

confidence: 99%

The novel long noncoding RNA CRART16 confers cetuximab resistance in colorectal cancer cells by enhancing ERBB3 expression via miR-371a-5p

et al. 2020

View full text Add to dashboard Cite

show abstract

“…In recent years, accumulating studies highlight the crucial roles of lncRNAs in the tumorigenesis of many human tumors . Among those lncRNAs, MIAT, a novel lncRNA, was found to be dysregulated and to promote malignancy in various cancers.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

et al. 2019

View full text Add to dashboard Cite

The aberrant expression of long non‐coding RNAs (lncRNAs) has been involved in the progression of many human tumors including osteosarcoma (OS). However, the biological function and the underlying mechanism of the lncRNA myocardial infarction‐associated transcript (MIAT) in OS remain unclear. In the present study, we found that lncRNA MIAT was significantly up‐regulated in both OS tissues and cell lines, and high expression of MIAT was positively associated with tumor size and lymph node metastasis of OS patients. In addition, knockdown of MIAT inhibited proliferation, migration, invasion and promoted apoptosis of OS cells in vitro. Moreover, the expression of MIAT was negatively associated with miR‐128‐3p but positively correlated with vascular endothelial growth factor C (VEGFC) in OS. Further mechanistic study revealed that lncRNA MIAT promoted OS progression by up‐regulating VEGFC via sponging miR‐128‐3p in vitro. Taken together, our results suggest that MIAT/miR‐128‐3p/VEGFC axis contributes to OS progression and may be used as a novel therapeutic target for OS. © 2019 IUBMB Life, 9999(9999):1–9, 2019

show abstract

“…Increasing evidence showed that lncRNAs exert functional role via activating Wnt pathway. For example, lncRNA NEAT1 promotes proliferation and metastasis in colorectal cancer via enhancing Wnt pathway . lncRNA DSCR8 facilitates cell cycle in hepatocellular carcinoma through the activation of Wnt pathway …”

Section: Discussionmentioning

confidence: 99%

“…For example, lncRNA NEAT1 promotes proliferation and metastasis in colorectal cancer via enhancing Wnt pathway. 42 lncRNA DSCR8 facilitates cell cycle in hepatocellular carcinoma through the activation of Wnt pathway. 43 The current research depicted that the knockdown of NNT-AS1 suppressed the relevant genes of Wnt pathway and restrained the activity and translocation of β-catenin (CTNNB1) in BC.…”

Section: Discussionmentioning

confidence: 99%

NNT‐AS1 enhances bladder cancer cell growth by targeting miR‐1301‐3p/PODXL axis and activating Wnt pathway

Liu

2019

Neurourology and Urodynamics

View full text Add to dashboard Cite

As a tumor involved in the urinary system, bladder cancer (BC) seriously threatens human health. Emerging as crucial biomarkers, long noncoding RNAs (lncRNAs) play an important role in the regulation of many cancers. lncRNA NNT-AS1 has been studied in a series of cancers, whereas its role and potential molecular mechanism was poorly understood in BC. Here, we found that NNT-AS1 was upregulated in BC cells. Functionally, the silencing of NNT-AS1 inhibited cell proliferation, migration, invasion, and endothelial-mesenchymal transition. Furthermore, the apoptosis of BC cells was induced upon NNT-AS1 knockdown. Later, miR-1301-3p, the downstream gene of NNT-AS1, was found at a low level in BC cells. In addition, we found that miR-1301-3p targeted to PODXL. PODXL expression downregulated in NNT-AS1-silenced cells was restored by miR-1301-3p inhibition. Importantly, NNT-AS1 was discovered to activate Wnt pathway, and the treatment of LiCl recovered the repressive role of NNT-AS1 silencing in BC cell growth. Through restoration assays, we observed that PODXL overexpressing countervailed NNT-AS1 depletionmediated suppression on BC cell growth and Wnt pathway. These data suggested that NNT-AS1 enhances BC cell growth and activates Wnt pathway by targeting miR-1301-3p/PODXL axis. K E Y W O R D Sbladder cancer, miR-1301-3p, NNT-AS1, PODXL

show abstract

Long non-coding RNA NEAT1 promotes colorectal cancer progression by competitively binding miR-34a with SIRT1 and enhancing the Wnt/β-catenin signaling pathway

Cited by 117 publications

References 28 publications

The novel long noncoding RNA CRART16 confers cetuximab resistance in colorectal cancer cells by enhancing ERBB3 expression via miR-371a-5p

The novel long noncoding RNA CRART16 confers cetuximab resistance in colorectal cancer cells by enhancing ERBB3 expression via miR-371a-5p

LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

NNT‐AS1 enhances bladder cancer cell growth by targeting miR‐1301‐3p/PODXL axis and activating Wnt pathway

Contact Info

Product

Resources

About