Evidence map›Paper›PMID 35241106›Full record

ArticleJournal of translational medicine2022

Activation of miR-500a-3p/CDK6 axis suppresses aerobic glycolysis and colorectal cancer progression.

Yu Liu, Wentao Tang, Li Ren, Tianyu Liu, Meng Yang, Ye Wei, Yijiao Chen, Meiling Ji, Guosong Chen, Wenju Chang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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  8. High expression of glycolysis-relatedJournal of thoracic disease · 2022
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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

11 authors at 2 institutions in 1 country.

Yu Liu *Colorectal Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Wentao Tang *Colorectal Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Li Ren *Colorectal Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Tianyu Liu *Colorectal Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Meng YangNational Clinical Research Center for Cancer, Tianjin Cancer Institute, Tianjin, China.
Ye WeiColorectal Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Yijiao ChenColorectal Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Meiling JiColorectal Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Guosong ChenThe State Key Laboratory of Molecular Engineering of Polymers and Department of Macromolecular Science, Shanghai, China.
Wenju ChangColorectal Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China. chang_erich@hotmail.com.
Jianmin XuColorectal Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China. xujmin@aliyun.com.ORCID 0000-0001-5441-8240
Sun Yat-sen University · CNTianjin Medical University Cancer Institute and Hospital · CN

Funding

Clinical Research Plan of SHDC SHDC2020CR1033BClinical Research Plan of SHDC SHDC2020CR3037BClinical Research Plan of SHDC SHDC2020CR5006National Natural Science Foundation of China 81602035National Natural Science Foundation of China 82072653National Natural Science Foundation of China 82072678Shanghai Engineering Research Center of Colorectal Cancer Minimally Invasive 17DZ2252600Shanghai Science and Technology Committee Project 19511121300Youth fund of Zhongshan Hospital 2019ZSQN28
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is one of the lethal cancers with a high mortality rate worldwide and understanding the mechanisms behind its progression is critical for improving patients' prognosis and developing therapeutics. MiR-500a-3p has been demonstrated to be involved in the progression of several human cancers but its role in CRC remains unclear. The aim of this study is to uncover the expression pattern and mechanisms of action of miR-500a-3p during the CRC progression.

methodsThe expression of miR-500a-3p and Cyclin-dependent kinases 6 (CDK6) in 134 CRC tissues were tested by quantitative PCR (qPCR) and immunohistochemistry staining (IHC), respectively. The effect of miR-500a-3p on cell proliferation was explored in vitro and in vivo. The glycolysis of CRC cells was determined by Mass Spectrometry and Seahorse XF 96 Extracellular Flux Analyzer. A dual-luciferase reporter assay was performed to validate the relationship between miR-500a-3p and CDK6.

resultsmiR-500a-3p was abnormally downregulated in CRC tissues and cell lines and was negatively associated with a worse prognosis. miR-500a-3p mimics impeded CRC cell proliferation in vitro and in vivo. miR-500a-3p inhibited glucose consumption, lactate and ATP production, and down-regulated the expression of hexokinase2 (HK2). In silico prediction combined with western blot and luciferase assay confirmed that CDK6 is a direct target of miR-500a-3p. Overexpression of CDK6 phenotypically rescued the inhibitory effect of miR-500a-3p on the proliferation and glycolysis of CRC cells.

conclusionsOur study revealed a potential tumor-suppressive role of miR-500a-3p in CRC, specifically targeting CDK6 and inhibiting cancer cell proliferation and aerobic glycolysis, which may provide new insights into novel prognostic biomarkers and therapeutic targets for CRC.

Indexed as

Colorectal NeoplasmsMicroRNAsCell ProliferationCyclin-Dependent Kinase 6GlycolysisHumansPrognosisCDK6 protein, humanCyclin-Dependent Kinase 6MicroRNAsCDK6Colorectal cancerGlycolysismiR-500a-3p

Identifiers

PMID35241106
PMCPMC8896266
OpenAlexW4214848910

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.