Evidence map›Paper›PMID 31040699›Full record

ArticleOncoTargets and therapy2019

LncRNA PVT1 promotes proliferation, invasion and epithelial-mesenchymal transition of renal cell carcinoma cells through downregulation of miR-16-5p.

Yu Ren, Weiping Huang, Guobin Weng, Pinger Cui, Haote Liang, Yeping Li

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 46 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Yu RenDepartment of Urology, Ningbo Urology and Nephrology Hospital, Ningbo 315000, Zhejiang Province, People's Republic of China.
Weiping HuangDepartment of Urology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, People's Republic of China, seasky13@126.com.
Guobin WengDepartment of Urology, Ningbo Urology and Nephrology Hospital, Ningbo 315000, Zhejiang Province, People's Republic of China.
Pinger CuiDepartment of Urology, Ningbo Urology and Nephrology Hospital, Ningbo 315000, Zhejiang Province, People's Republic of China.
Haote LiangDepartment of Urology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, People's Republic of China, seasky13@126.com.
Yeping LiDepartment of Urology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, People's Republic of China, seasky13@126.com.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLncRNAs have recently emerged as vital regulators in the pathogenesis and development of various cancers. LncRNA PVT1 is reported to function as an oncogene in some tumors. However, the role of PVT1 in RCC remains unknown. PURPOSE: To explore the potential effects of lncPVT1 on the development of renal cell carcinoma.

methodsThe expression of PVT1 in renal cancer cell lines and tissues was measured by qRT-PCR. The endogenous PVT1 was silenced by RNAi. Cell viabilities were measured by the MTT assay. The migration and invasion of cells were investigated by the transwell assay. The apoptosis of cells was measured by the Nucleosome ELISA and caspase-3 activity assays. The levels of proteins were measured by the western blot.

resultsWe found that PVT1 was upregulated in RCC tissues compared with the adjacent normal tissues. PVT1 expression was closely correlated with TNM stage, Fuhrman grade, lymph node metastasis and tumor size. Kaplan-Meier analysis revealed that high expression of PVT1 was significantly associated with poor overall survival. In accordance, overexpression of PVT1 was observed in RCC cells comto HK-2 cell. Silencing of PVT1 significantly repressed cell viability, induced apoptosis and inhibited cell migration and invasion in vitro. Furthermore, bioinformatic analysis and luciferase reporter assay confirmed that miR-16-5p was a target of PVT1. Silencing of miR-16-5p mostly reversed the regulatory effects on RCC cells induced by downregulation of PVT1.

conclusionIn summary, our study indicates that targeting PVT1 might represent a rational therapeutic strategy for RCC.

Indexed as

apoptosisinvasionmigrationmiR-16-5pPVT1renal carcinoma

Identifiers

PMID31040699
PMCPMC6454988
OpenAlexW2928240819

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.