Evidence map›Paper›PMID 34423392›Full record

ArticleJournal of physiology and biochemistry2021

Exosome-derived SNHG16 sponging miR-4500 activates HUVEC angiogenesis by targeting GALNT1 via PI3K/Akt/mTOR pathway in hepatocellular carcinoma.

Shuangda Li, Yu Qi, Yiran Huang, Yanru Guo, Tong Huang, Li Jia

Abstract read
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In one paragraph

Article in Journal of physiology and biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 49 citations in OpenAlex.

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  17. Exosomal microRNA as a key regulator of PI3K/AKT pathways in human tumors.Medical oncology (Northwood, London, England) · 2024
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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

6 authors at 1 institution in 1 country.

Shuangda Li *College of Laboratory Medicine, Dalian Medical University, 9 Lvshunnan Road Xiduan, Dalian, 116044, Liaoning Province, China.
Yu Qi *College of Laboratory Medicine, Dalian Medical University, 9 Lvshunnan Road Xiduan, Dalian, 116044, Liaoning Province, China.
Yiran HuangCollege of Laboratory Medicine, Dalian Medical University, 9 Lvshunnan Road Xiduan, Dalian, 116044, Liaoning Province, China.
Yanru GuoCollege of Laboratory Medicine, Dalian Medical University, 9 Lvshunnan Road Xiduan, Dalian, 116044, Liaoning Province, China.
Tong HuangCollege of Laboratory Medicine, Dalian Medical University, 9 Lvshunnan Road Xiduan, Dalian, 116044, Liaoning Province, China.
Li JiaCollege of Laboratory Medicine, Dalian Medical University, 9 Lvshunnan Road Xiduan, Dalian, 116044, Liaoning Province, China. linjian0198@sina.com.ORCID http://orcid.org/0000-0002-3286-444X
Dalian Medical University · CN

Funding

National Natural Science Foundation of China 81772277
6 · The paper itself

Abstract

Accumulating evidence suggests cancer-derived exosomes play an important role in promoting angiogenesis. Long noncoding RNA small nucleolar RNA host gene 16 (SNHG16) is known to aggravate hepatocellular carcinoma (HCC) progression. However, the function of exosomal SNHG16 in HCC angiogenesis remains unclear. In this study, the expression of SNHG16 was significantly upregulated in HCC tissues and cell lines. The proliferative, migratory, and angiogenic abilities of HUVECs were enhanced after exposure to exosomes derived from HCC cells by transmitting SNHG16. In addition, SNHG16 was validated to promote the biological function of HUVECs directly. Exosomal SNHG16 increased GALNT1 expression to promote angiogenesis via sponging miR-4500. SNHG16/miR-4500/GALNT1 axis played an important role in exosome-mediated angiogenesis and tumor growth in vitro and vivo. Furthermore, SNHG16 activated PI3K/Akt/mTOR pathway via competing endogenous miR-4500 and GALNT1. Meanwhile, the expression of plasma exosomal SNHG16 upregulated in the plasma of HCC patients. These data elucidated the essential role of exosomal SNHG16 in communication between HCC cells and endothelial cells. Exosomal SNHG16 could be utilized as a therapeutic target for anti-angiogenesis in HCC progression.

Indexed as

Carcinoma, HepatocellularExosomesLiver NeoplasmsMicroRNAsRNA, Long NoncodingCell Line, TumorCell ProliferationEndothelial CellsGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesMicroRNAsMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingTOR Serine-Threonine KinasesAngiogenesisExosomal SNHG16GALNT1HCCmiR-4500PI3K/Akt/mTOR pathway

Identifiers

PMID34423392
OpenAlexW3193532839

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.