Evidence map›Paper›PMID 34110962›Full record

ArticleRNA biology2021

MIR210HG regulates glycolysis, cell proliferation, and metastasis of pancreatic cancer cells through miR-125b-5p/HK2/PKM2 axis.

Tianzhu Yu, Guoping Li, Chenggang Wang, Gaoquan Gong, Liangwen Wang, Changyu Li, Yi Chen, Xiaolin Wang

Open access · bronzeAbstract read
In one paragraph

Article in RNA biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  9. Review
  10. Emerging Roles of ncRNAs Regulating PKM2 in Cancer Progression.Current pharmaceutical biotechnology · 2025
    Review
  11. Review
  12. MIR210HG Accelerates the Progression of Colorectal Cancer and Affects the Function of Colorectal Cancer Cells by Downregulating miR-1226-3p.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
  13. LncRNAAsian journal of urology · 2024
    Article
  14. Article
  15. Review
  16. Review
  17. Article
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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

8 authors at 3 institutions in 1 country.

Tianzhu YuDepartment of Interventional Radiology, Zhongshan Hospital, Fudan University, Shanghai, China.
Guoping LiDepartment of Interventional Radiology, Zhongshan Hospital, Fudan University, Shanghai, China.
Chenggang WangDepartment of Interventional Radiology, Zhongshan Hospital, Fudan University, Shanghai, China.
Gaoquan GongDepartment of Interventional Radiology, Zhongshan Hospital, Fudan University, Shanghai, China.
Liangwen WangDepartment of Interventional Radiology, Zhongshan Hospital, Fudan University, Shanghai, China.
Changyu LiDepartment of Interventional Radiology, Zhongshan Hospital, Fudan University, Shanghai, China.
Yi ChenDepartment of Interventional Radiology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaolin WangDepartment of Interventional Radiology, Zhongshan Hospital, Fudan University, Shanghai, China.
Shanghai Institute of Hematology · CNZhongshan Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer has the worst prognosis of all common cancers. Pancreatic cancer cells have a metabolic advantage due to their swiftly adaptive responses to hypoxic and low-nutrient medium. This advantage contributes to the aggressivity of pancreatic cancer. In this study, lncRNA MIR210HG was abnormally upregulated within pancreatic cancer. It acted as a key oncogenic regulator of pancreatic cancer aggressiveness and glycolysis. Knockdown of MIR210HG significantly inhibited the aggressive phenotype of pancreatic cancer cells and inhibited the growth of xenograft tumours. More importantly, MIR210HG knockdown inhibited pancreatic cancer cell glycolysis via regulating the glycolysis-related hexokinase 2 (HK2) and Pyruvate kinase muscle isozyme M2 (PKM2) expression. Compared with the MIR210HG knockdown group, miR-125b-5p inhibition promoted the aggressive phenotypes and glycolysis of pancreatic cancer cells. Furthermore, the effects of MIR210HG knockdown on HK2 and PKM2 expression, pancreatic cancer cell aggressive phenotypes, and glycolysis were significantly reversed by miR-125b-5p inhibition. In tissue samples, MIR210HG expression was negatively correlated with miR-125b-5p levels and positively correlated with HK2 and PKM2 expression. miR-125b-5p expression was negatively correlated with HK2 and PKM2 expression. In conclusion, MIR210HG affected the phenotypes of pancreatic cancer cells, including proliferation, invasion, migration, and glycolysis, via modulating the miR-125b-5p/HK2/PKM2 axis.

Indexed as

Gene Expression Regulation, NeoplasticGlycolysisCarrier ProteinsCell MovementCell ProliferationHexokinaseHumansMembrane ProteinsMicroRNAsNeoplasm MetastasisPancreatic NeoplasmsRNA, Long NoncodingThyroid Hormone-Binding ProteinsThyroid HormonesTumor Cells, CulturedCarrier ProteinsHexokinaseHK2 protein, humanMembrane ProteinsMicroRNAsMIRN125 microRNA, humanRNA, Long NoncodingThyroid Hormone-Binding ProteinsThyroid HormonesHK2lncRNA MIR210HGmetabolic reprogrammingmiR-125b-5pPancreatic cancerPKM2

Identifiers

PMID34110962
PMCPMC8632125
OpenAlexW3169399514

What OpenQuestion holds

Textmetadata
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.