Long noncoding RNA PVT1 promotes laryngeal squamous cell carcinoma development by acting as a molecular sponge to regulate miR‐519d‐3p

Zheng, Xiling; Zhao, Kang; Liu, Tao; Liu, Lei; Zhou, Changming; Xu, Min

doi:10.1002/jcb.27673

Cited by 25 publications

(18 citation statements)

References 33 publications

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“…Consistently, PVT1 is overexpressed in cancer cells compared to normal non-tumorigenic epithelial cells. It is found to be upregulated in bladder (24), breast (25–27), cervical (28), colon (29), colorectal (30, 31), gastric (32–35), lung (36–41), pancreatic (42), and prostate cancer (43–46), as well as clear cell renal cell carcinoma (18), esophageal squamous cell carcinoma (SCC) (20, 47), glioma (48–50), head and neck SCC, hepatocellular carcinoma (51–55), laryngeal SCC (56), malignant pleural mesothelioma (57), osteosarcoma (58–60), and papillary thyroid carcinoma (61), melanoma (62). Further, data from The Cancer Genome Atlas (TCGA) and independent analysis of human clinical tissue samples showed elevated PVT1 expression in cancer tissues in comparison to adjacent normal tissue or matched normal tissue (27, 31, 32, 45, 50).…”

Section: Biological Significance Of Pvt1mentioning

confidence: 99%

PVT1 Signaling Is a Mediator of Cancer Progression

et al. 2019

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There is increasing evidence that PVT1 has oncogenic properties and regulates proliferation and growth of many cancers. Themolecular mechanisms of action of PVT1 are mediated, in part, by microRNAs (miRNAs). However, some well-established transcription factors involved in cancer cell proliferation share a common thread of microRNA associations with PVT1. Furthermore, these microRNAs are also involved in mechanisms that lead to the development of drug resistance in cancer cells. While several microRNAs have been implicated directly in PVT1-mediated tumorigenesis, significant steps need to be taken to elucidate these important relationships. We synthesize the current knowledge of the miRNAs and associated genes by which PVT1 contributes to tumorigenesis. Overall, the trend suggests a negative correlation of microRNA expression with PVT1. It is clear that future studies involving PVT1 should be carried out in conjunction with microRNA analysis and should include large scale lncRNA-miRNA-mRNA network analysis. Likewise, the relationship between established transcription factors such as p53 and MYC , and processes like epithelial-mesenchymal transition may offer valuable insight into the yet unknown mechanisms of PVTI-mediated cancer progression via microRNA-dependent signaling networks.

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Section: Biological Significance Of Pvt1mentioning

confidence: 99%

PVT1 Signaling Is a Mediator of Cancer Progression

et al. 2019

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“…PVT1 functions as a molecular sponge to competitively inhibit miRNAs, including miR-448, miR-195, miR-497, miR-20a-5p [6], [9], [12], [20], [23]. PVT1 has been reported to sponge miR-519d-3p to facilitate invasion and proliferation in laryngeal squamous cell cancer [15]. We speculated that PVT1 may facilitate PDAC progression and glycolysis through down regulation of miR-519d-3p.…”

Section: Discussionmentioning

confidence: 98%

“…International Publisher laryngeal squamous cell cancer [15]. However, the mechanism of PVT1 by regulating the miR-519d-3p/ HIF-1 in cell metabolism remains largely unknown.…”

Section: Ivyspringmentioning

confidence: 99%

Upregulation of LncRNA PVT1 Facilitates Pancreatic Ductal Adenocarcinoma Cell Progression and Glycolysis by Regulating MiR-519d-3p and HIF-1A

et al. 2020

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The long, noncoding RNA (lncRNA) PVT1, as an important epigenetic regulator, has a critical role in carcinogenesis. However, its role in pancreatic ductal adenocarcinoma (PDAC) has not been fully investigated. Here, the up-regulated expression of lncRNA PVT1 is found in our PDAC tumor samples. Knockdown of it suppressed PDCA cells growth and glycolysis. An inverse association between miR-519d-3p and PVT1 was found. RIP, RNA pulldown and luciferase assay showed that PVT1 directly targets miR-519d-3p by binding with microRNA binding site. Bioinformatics analysis and study indicated that HIF-1A is a target of miR-519d-3p. Collectively, our findings suggested that PVT1 could act as an oncogenic lncRNA, and promote tumor progression by regulating HIF-1A via competing with miR-519d-3p.

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“…32 LncRNAs act as sponges of small RNAs and eliminate their inhibitory effects in many cancers. For instance, the lncRNA PVT1 acts as a molecular sponge regulates the expression miR-519d-3p 33 and promotes the development of laryngeal cancer. Huang et al reported that lncRNA near 1 promotes pancreatic cancer progression by acting as a ceRNA of miR-506-3p.…”

Section: Discussionmentioning

confidence: 99%

<p>Long-Noncoding RNA PCAT6 Aggravates Osteosarcoma Tumourigenesis via the MiR-143-3p/ZEB1 Axis</p>

Wu¹,

Feng²,

Li³

et al. 2020

OTT

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The long-noncoding RNA PCAT6 plays an important regulatory role in the development of several cancers. However, the expression pattern and underlying mechanisms of PCAT6 in osteosarcoma (OS) are yet unknown. Methods: We used real-time PCR to measure PCAT6 expression in 106 tumor pairs and corresponding non-tumor tissues from OS patients. Statistical analyses were applied to evaluate the prognostic value and associations of PCAT6 expression with clinical parameters. Furthermore, the PCAT6 was silenced with siRNA in OS cells. Moreover, phenotype of PCAT6 silenced OS cells was measured using colony formation, CCK-8, cell migration and invasion assay. Finally, the molecular mechanism of PCAT6/miR-143-3p/ZEB1 axis in OS progression was explored. Results: The expression level of PCAT6 in OS tissues was significantly elevated as compared with that in the adjacent normal bone tissues and that high PCAT6 expression closely correlated with the malignant phenotype and poor survival among patients with OS. Multivariate analyses revealed PCAT6 overexpression as an independent prognostic factor for the poor outcome of patients with OS. Functional assay results demonstrated that the knockdown of PCAT6 expression notably suppressed the proliferation, migration, and invasion of OS cells. An elevated PCAT6 level aggravated the malignant phenotype of OS cells via ZEB1 expression upregulation. Mechanistic studies revealed that PCAT6 could sponge endogenous miR-143-3p and inhibit its activity, resulting in an increase in ZEB1 level. Finally, we demonstrated that the tumour-promoting role of PCAT6 in OS was dependent on the regulation of the miR-143-3p/ZEB1 axis. Conclusion: These findings highlight the potential role of PCAT6, which could serve as a valuable prognostic indicator for patients with OS.

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Long noncoding RNA PVT1 promotes laryngeal squamous cell carcinoma development by acting as a molecular sponge to regulate miR‐519d‐3p

Cited by 25 publications

References 33 publications

PVT1 Signaling Is a Mediator of Cancer Progression

PVT1 Signaling Is a Mediator of Cancer Progression

Upregulation of LncRNA PVT1 Facilitates Pancreatic Ductal Adenocarcinoma Cell Progression and Glycolysis by Regulating MiR-519d-3p and HIF-1A

<p>Long-Noncoding RNA PCAT6 Aggravates Osteosarcoma Tumourigenesis via the MiR-143-3p/ZEB1 Axis</p>

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