Down-regulating NEAT1 inhibited the viability and vasculogenic mimicry formation of sinonasal squamous cell carcinoma cells via miR-195-5p/VEGFA axis

Lu, Honglue; Kang, Fei

doi:10.1042/bsr20201373

Cited by 12 publications

(5 citation statements)

References 35 publications

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“…A study on the molecular mechanisms of SNSCC development revealed that the expression of lncRNA NEAT1 and vascular endothelial growth factor A (VEGFA) were both upregulated in SNSCC tissues and cells, which resulted in a promotion of SNSCC cell viability and a reduction in SNSCC cell apoptosis. Moreover, upregulation of miR-195-5p in SNSCC cells decreased cell viability by directly binding with NEAT1 and VEGFA and decreasing their expression levels, suggesting an important role of the NEAT1/miR-195-5p/VEGFA axis in SNSCC progression [25].…”

Section: Sinonasal Squamous Cell Carcinomamentioning

confidence: 97%

NEAT1 as a competing endogenous RNA in tumorigenesis of various cancers: Role, mechanism and therapeutic potential

Yao

et al. 2021

Int. J. Biol. Sci.

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The nuclear paraspeckle assembly transcript 1 (NEAT1) is a long non-coding RNA (lncRNA) that is upregulated in a variety of human cancer types. Increasing evidence has shown that the elevation of NEAT1 in cancer cells promotes cell growth, migration, and invasion and inhibits cell apoptosis. It is also known that lncRNAs act as a competing endogenous RNA (ceRNA) by sponging microRNAs (miRNAs) to alter the expression levels of their target genes in the development of cancers. Therefore, it is important to understand the molecular mechanisms underlying this observation. In this review, specific emphasis was placed on NEAT1's role in tumor development. We also summarize and discuss the feedback roles of NEAT1/miRNA/target network in the progression of various cancers. As our understanding of the role of NEAT1 during tumorigenesis improves, its therapeutic potential as a biomarker and/or target for cancer also becomes clearer.

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Section: Sinonasal Squamous Cell Carcinomamentioning

confidence: 97%

NEAT1 as a competing endogenous RNA in tumorigenesis of various cancers: Role, mechanism and therapeutic potential

Yao

et al. 2021

Int. J. Biol. Sci.

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“…For instance, according to the literature, miR-195–5p is a promising biomarker and a potential therapeutic target for the development of anticancer drugs . By blocking PI3K/AKT, MAPK, TNF, Hippo, Wnt/β-catenin, JAK–STAT, and Notch signaling pathways, miR-195–5p represses the proliferation, migration, and invasiveness of tumor cells in cancers of various organs. − This miRNA has been reported to regulate the proliferation, invasiveness, and apoptosis of cells of thyroid cancer and melanoma through an impact on the expression of the TERT gene. Moreover, it has been shown that due to its effect on a MYC-binding protein, miR-195–5p can inhibit transcriptional activity of stemness gene MYC …”

Section: Discussionmentioning

confidence: 99%

Prevention of Metastasis by Suppression of Stemness Genes Using a Combination of microRNAs

Nevskaya,

Pershina,

Hmelevskaya

et al. 2024

J. Med. Chem.

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We propose an original strategy for metastasis prevention using a combination of three microRNAs that blocks the dedifferentiation of cancer cells in a metastatic niche owing to the downregulation of stemness genes. Transcriptome microarray analysis was applied to identify the effects of a mixture of microRNAs on the pattern of differentially expressed genes in human breast cancer cell lines. Treatment of differentiated CD44– cancer cells with the microRNA mixture inhibited their ability to form mammospheres in vitro. The combination of these three microRNAs encapsulated into lipid nanoparticles prevented lung metastasis in a mouse model of spontaneous metastasis. The mixture of three microRNAs (miR-195–5p/miR-520a/miR-630) holds promise for the development of an antimetastatic therapeutic that blocks tumor cell dedifferentiation, which occurs at secondary tumor sites and determines the transition of micrometastases to macrometastases.

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“…The potential regulatory mechanism is associated with some critical signaling molecules involved in tumor metastasis, invasion, and matrix reconstruction, such as vascular endothelial cadherin (VE‐cadherin), VEGFA, EphA2, PI3K/AKT signals, MMPs, and HIF‐1α. In this context, VEGFA has been reported to regulate the proliferation, migration, and survival of vascular endothelial cells by activating its receptor VEGFR2 on vascular endothelial cells [ 59 ], as well as positively regulating angiogenesis and VM formation [ 60 ]. In addition, MMPs, which are known as critical regulators in glioma invasion [ 61 ], have been found to be potential biomarkers of VM formation in lung cancer and melanoma [ 62 , 63 , 64 ].…”

Section: Discussionmentioning

confidence: 99%

L1CAM promotes vasculogenic mimicry formation by miR‐143‐3p‐induced expression of hexokinase 2 in glioma

et al. 2023

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In recent decades, antiangiogenic therapy, which blocks the supply of oxygen and nutrition to tumor cells, has become a promising clinical strategy for the treatment of patients with tumors. However, recent studies revealed that vasculogenic mimicry (VM), which is the process by which vascular morphological structures are formed by highly invasive tumor cells, has been considered a potential factor for the failure of antiangiogenic therapy in patients with tumors. Thus, inhibition of VM formation might be a potential target for improving the outcome of antiangiogenic strategies. However, the mechanism underlying VM formation is still incompletely elucidated. Herein, we report that L1CAM might be a critical regulator of VM formation in glioma, and might be associated with the resistance of glioma to antiangiogenic therapy. We found that the tumor‐invasion and tube‐formation capabilities of L1CAM ‐overexpressing cells were significantly enhanced in vitro and in vivo . In addition, the results indicated that miR‐143‐3p, which might directly target the 3'UTR of the hexokinase 2 ( HK2 ) gene to regulate its protein expression, was subsequently involved in L1CAM‐mediated VM formation by glioma cells. Further study revealed that the regulation of MMP2 , MMP9, and VEGFA expression was involved in this process. Moreover, we identified that activation of the downstream PI3K/AKT signaling pathway of the L1CAM/HK2 cascade is critical for VM formation by glioma cells. Furthermore, we found that the combined treatment of anti‐L1CAM neutralizing monoclonal antibody and bevacizumab increases efficacy beyond that of bevacizumab alone, and suppresses glioma growth in vivo , indicating that the inhibition of L1CAM‐mediated VM formation might efficiently improve the effect of antiangiogenic treatment for glioma patients. Together, our findings demonstrated a critical role of L1CAM in regulating VM formation in glioma, and that L1CAM might be a potential target for ameliorating tumor resistance to antiangiogenic therapy in glioma patients.

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Down-regulating NEAT1 inhibited the viability and vasculogenic mimicry formation of sinonasal squamous cell carcinoma cells via miR-195-5p/VEGFA axis

Cited by 12 publications

References 35 publications

NEAT1 as a competing endogenous RNA in tumorigenesis of various cancers: Role, mechanism and therapeutic potential

NEAT1 as a competing endogenous RNA in tumorigenesis of various cancers: Role, mechanism and therapeutic potential

Prevention of Metastasis by Suppression of Stemness Genes Using a Combination of microRNAs

L1CAM promotes vasculogenic mimicry formation by miR‐143‐3p‐induced expression of hexokinase 2 in glioma

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