Evidence map›Paper›PMID 34382305›Full record

ArticleCancer science2021

Methylation-associated silencing of miR-9-1 promotes nasopharyngeal carcinoma progression and glycolysis via HK2.

Qian-Lan Xu, Zan Luo, Bin Zhang, Guan-Jie Qin, Ru-Yun Zhang, Xiang-Yun Kong, Hua-Ying Tang, Wei Jiang

Abstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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  11. Decoding the regulatory roles of non-coding RNAs in cellular metabolism and disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  12. The Mechanism of DNA Methylation and miRNA in Breast Cancer.International journal of molecular sciences · 2023
    Review
  13. Review
  14. Article
  15. 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

8 authors.

Qian-Lan XuDepartment of Radiation Oncology, Affiliated Hospital of Guilin Medical University, Guilin, China.
Zan LuoDepartment of Radiation Oncology, Affiliated Hospital of Guilin Medical University, Guilin, China.
Bin ZhangDepartment of Radiation Oncology, Wuzhou Red Cross Hospital, Wuzhou, China.
Guan-Jie QinDepartment of Radiation Oncology, Affiliated Hospital of Guilin Medical University, Guilin, China.
Ru-Yun ZhangDepartment of Radiation Oncology, Affiliated Hospital of Guilin Medical University, Guilin, China.
Xiang-Yun KongDepartment of Radiation Oncology, Affiliated Hospital of Guilin Medical University, Guilin, China.
Hua-Ying TangDepartment of Radiation Oncology, Affiliated Hospital of Guilin Medical University, Guilin, China.
Wei JiangDepartment of Radiation Oncology, Affiliated Hospital of Guilin Medical University, Guilin, China.ORCID https://orcid.org/0000-0001-6534-8612

Funding

Chinese Society of Clinical Oncology Y-Young2020-0520General Program of Guangxi Natural Science Foundation of China 2018GXNSFAA138100Key Program of the Guangxi Natural Science Foundation of China 2018JJD140054National Natural Science Foundation of China 81560443National Natural Science Foundation of China 81760546
6 · The paper itself

Abstract

Characteristically, cancer cells metabolize glucose through aerobic glycolysis, known as the Warburg effect. Accumulating evidence suggest that during cancer formation, microRNAs (miRNAs) could regulate such metabolic reprogramming. In the present study, miR-9-1 was identified as significantly hypermethylated in nasopharyngeal carcinoma (NPC) cell lines and clinical tissues. Ectopic expression of miR-9-1 inhibited NPC cell growth and glycolytic metabolism, including reduced glycolysis, by reducing lactate production, glucose uptake, cellular glucose-6-phosphate levels, and ATP generation in vitro and tumor proliferation in vivo. HK2 (encoding hexokinase 2) was identified as a direct target of miR-9-1 using luciferase reporter assays and Western blotting. In NPC cells, hypermethylation regulates miR-9-1 expression and inhibits HK2 translation by directly targeting its 3' untranslated region. MiR-9-1 overexpression markedly reduced HK2 protein levels. Restoration of HK2 expression attenuated the inhibitory effect of miR-9-1 on NPC cell proliferation and glycolysis. Fluorescence in situ hybridization results indicated that miR-9-1 expression was an independent prognostic factor in NPC. Our findings revealed the role of the miR-9-1/HK2 axis in the metabolic reprogramming of NPC, providing a potential therapeutic strategy for NPC.

Indexed as

3' Flanking RegionAdenosine TriphosphateAnimalsCell Line, TumorCell ProliferationDisease ProgressionGlucoseGlucose-6-PhosphateGlycolysisHeterograftsHexokinaseHumansIn Situ Hybridization, FluorescenceLactic AcidMaleMethylationAdenosine TriphosphateGlucoseGlucose-6-PhosphateHexokinaseHK2 protein, humanLactic AcidMicroRNAsMIRN92 microRNA, humanRNA, Messengerglycolysis metabolismHK2methylationmicroRNA-9-1nasopharyngeal carcinoma

Identifiers

PMID34382305
PMCPMC8486208

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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.