Evidence map›Paper›PMID 31819647›Full record

ArticleCancer management and research2019

HIF1α/miR-520a-3p/AKT1/mTOR Feedback Promotes The Proliferation And Glycolysis Of Gastric Cancer Cells.

Chen Pan, Qi Liu, Xiaoling Wu

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

25 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  4. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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  8. Energy metabolism: a new target for gastric cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
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  13. The microRNA-520a-3p inhibits invasion and metastasis by targeting NF-kappaB signaling pathway in non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
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  19. Small RNAs, Big Diseases.International journal of molecular sciences · 2020
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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

3 authors at 2 institutions in 1 country.

Chen PanDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Qi LiuDepartment of Gastroenterology, The Affiliated Hospital of Guizhou Medical University, Guiyang, People's Republic of China.ORCID 0000-0001-5409-1356
Xiaoling WuDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Guiyang Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeVarious microRNAs are involved in the development of gastric cancer (GC). This study investigated the role and mechanism of miR-520a-3p in GC.

methodQuantitative real-time fluorescence PCR (qRT-PCR) was applied to measure the expression level of miR-520a-3p in GC tissues and cell lines. The chi-squared test was employed to evaluate the relationship between the expression level of miR-520a-30p and clinical traits. The cell count kit-8 assay was used to detect the effect of miR-520a-3p on GC cell proliferation, while its effect on glycolysis was determined using the glucose assumption, lactate, and ATP production assay. The effect of miR-520a-3p on tumor growth in vivo was examined using a xenograft model. The relationship between miR-520a-30p and AKT1/mTOR/HIF1α pathway in normoxia and hypoxia was investigated using bioinformatics analysis, dual-luciferase reporter assay, qRT-PCR and Western blotting.

resultsThe expression of miR-520a-3p was decreased in GC tissues and cell lines. The expression level of miR-520a-3p was negatively associated with various malignant biological properties in patients. Overexpression/inhibition of miR-520a-3p decreased/promoted cell proliferation and glycolysis in vitro. Overexpression of miR-520a-3p inhibited tumor growth in vivo. AKT1 is the functional target of MiR-520a-3p, which was decreased in miR-520a-3p-overexpressing cells. In addition, overexpression of miR-520a-3p decreased the protein level of AKT1, mTOR, HIF1α, and target genes of HIF1α such as Glut1 and VEGF. Restoration of the expression of AKT1 can decrease the inhibitory effect of miR-520a-3p on the AKT1/mTOR/HIF1α pathway, as well as cell proliferation and glycolysis. Furthermore, the level of miR-520a-3p was decreased, while that of AKT1 was increased under hypoxia. Notably, inhibition of HIF1α or overexpression of miR-520a-3p suppressed these effects.

conclusionOur study provided the first evidence for the existence of HIF1α/miR-520a-3p/AKT1/mTOR feedback, which promotes the proliferation and glycolysis of GC cells, highlighting a potential novel target for treatment.

Indexed as

AKT/mTOR/HIF1α pathwaygastric cancerglycolysismiR-520a-3p

Identifiers

PMID31819647
PMCPMC6897058
OpenAlexW2989607427

What OpenQuestion holds

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LicenceCC BY-NC
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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.