Evidence map›Paper›PMID 35073936›Full record

ArticleCancer cell international2022

Golgi phosphoprotein 3 promotes angiogenesis and sorafenib resistance in hepatocellular carcinoma via upregulating exosomal miR-494-3p.

Ying Gao, Zheng Yin, Yunling Qi, Hong Peng, Wenbin Ma, Ruizhi Wang, Wen Li

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  4. The highly expressedJournal of gastrointestinal oncology · 2025
    Article
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  6. Article
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  10. Article
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  13. Microvesicles: the functional mediators in sorafenib resistance.Cancer drug resistance (Alhambra, Calif.) · 2022
    Review
  14. Review
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

7 authors at 1 institution in 1 country.

Ying Gao *Laboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Zheng Yin *Laboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Yunling QiDivision of Vascular Surgery, National Guangdong Joint Engineering Laboratory for Diagnosis and Treatment of Vascular Diseases, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Hong PengCenter of hepato-pancreatobiliary surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Wenbin MaSchool of Life Sciences, Sun Yat-sen University, Guangzhou, 510275, China.
Ruizhi WangLaboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China. wangrzh3@mail.sysu.edu.cn.
Wen LiLaboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China. liwen@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-5262-1317
Sun Yat-sen University · CN

Funding

Key Programme 2018YFA0107003National Natural Science Foundation of China 31871479National Natural Science Foundation of China 81672417National Natural Science Foundation of China 81972750
6 · The paper itself

Abstract

backgroundGolgi phosphoprotein 3 (GOLPH3) has been frequently reported as an oncoprotein in a variety of tumors. However, its role in the cancer-associated intercellular signaling communication has not yet been explored. This study aimed at exploring whether GOLPH3 regulates angiogenesis and sorafenib resistance via exosomal mechanisms in hepatocellular carcinoma (HCC).

methodsIn vivo assays were performed to elucidate the function of GOLPH3 in HCC. Exosomes of HCC cells were isolated by differential centrifugation, and then measured and quantified using nanoparticle tracking analysis (NTA), BCA assay, western blot (WB), and transmission electron microscopy (TEM). Differentially expressed miRNAs in exosome were analyzed and verified through small RNA sequencing (sRNA-seq) and reverse-transcription polymerase chain reaction (RT-PCR). In addition, a series of in vitro assays were performed to determine the function of exosomes and miR-494-3p in HCC. The candidate target gene of miR-494-3p was identified by bioinformatics prediction and dual-luciferase reporter assay.

resultsDownregulation of GOLPH3 expression could suppress angiogenesis and enhance sorafenib sensitivity in HCC. Exosomes derived from GOLPH3 overexpression HCC cells promoted the angiogenesis ability of HUVECs and induced sorafenib resistance in HCC cells. A total of 13 differentially expressed miRNAs between negative control and GOLPH3 knockdown group were found in exosomes. However, GOLPH3 was only associated with miR-494-3p expression level in exosomes derived from HCC cells without affecting total cellular miR-494-3p content. Results confirmed that exosomal miR-494-3p promotes angiogenesis of HUVECs and sorafenib resistance in HCC cells through directly targeting PTEN.

conclusionsHCC cells with high expression levels of GOLPH3 could promote angiogenesis and sorafenib resistance by enhancing exosomal miR-494-3p secretion to recipient HUVECs and HCC cells, respectively.

Indexed as

AngiogenesisExosomal miR-494-3pGOLPH3Hepatocellular carcinomaSorafenib resistance

Identifiers

PMID35073936
PMCPMC8785582
OpenAlexW4207044591

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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.