Evidence map›Paper›PMID 30755600›Full record

ArticleCell death & disease2019

P53-induced miR-1249 inhibits tumor growth, metastasis, and angiogenesis by targeting VEGFA and HMGA2.

Xiaoxiang Chen, Kaixuan Zeng, Mu Xu, Xiangxiang Liu, Xiuxiu Hu, Tao Xu, Bangshun He, Yuqin Pan, Huiling Sun, Shukui Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

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5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Xiaoxiang ChenGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.
Kaixuan ZengGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.
Mu XuGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.
Xiangxiang LiuGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.
Xiuxiu HuGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.
Tao XuGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.
Bangshun HeGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.
Yuqin PanGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.
Huiling SunGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.
Shukui WangGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China. sk_wang@njmu.edu.cn.ORCID http://orcid.org/0000-0001-6972-2587
Nanjing Medical University · CNSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are important class of functional regulators involved in human cancers development, including colorectal cancer (CRC). Exploring aberrantly expressed miRNAs may provide us with new insights into the initiation and development of CRC by functioning as oncogenes or tumor suppressors. The aim of our study is to discover the expression pattern of miR-1249 in CRC and investigate its clinical significance as well as biological role in CRC progression. In our study, we found that miR-1249 was markedly downregulated in CRC tissues and cell lines, and negatively related to pN stage, pM stage, TNM stage, and overall survival (OS). Moreover, we demonstrated that miR-1249 was a direct transcriptional target of P53 and revealed that P53-induced miR-1249 inhibited tumor growth, metastasis and angiogenesis in vitro and vivo. Additionally, we verified that miR-1249 suppressed CRC proliferation and angiogenesis by targeting VEGFA as well as inhibited CRC metastasis by targeting both VEGFA and HMGA2. Further studying showed that miR-1249 suppressed CRC cell proliferation, migration, invasion, and angiogenesis via VEGFA-mediated Akt/mTOR pathway as well as inhibited EMT process of CRC cells by targeting both VEGFA and HMGA2. Our study indicated that P53-induced miR-1249 may suppress CRC growth, metastasis and angiogenesis by targeting VEGFA and HMGA2, as well as regulate Akt/mTOR pathway and EMT process in the initiation and development of CRC. miR-1249 might be a novel the therapeutic candidate target in CRC treatment.

Indexed as

AnimalsCell MovementCell ProliferationColorectal NeoplasmsDisease ProgressionFemaleHCT116 CellsHeterograftsHMGA2 ProteinHT29 CellsHumansHuman Umbilical Vein Endothelial CellsMaleMiceMice, Inbred BALB CMice, NudeHMGA2 ProteinHMGA2 protein, humanMicroRNAsTP53 protein, humanTumor Suppressor Protein p53Vascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID30755600
PMCPMC6372610
OpenAlexW2914178603

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.