Evidence map›Paper›PMID 31426130›Full record

ArticleCancer medicine2019

Hexokinase 2 dimerization and interaction with voltage-dependent anion channel promoted resistance to cell apoptosis induced by gemcitabine in pancreatic cancer.

Kun Fan, Zhiyao Fan, He Cheng, Qiuyi Huang, Chao Yang, Kaizhou Jin, Guopei Luo, Xianjun Yu, Chen Liu

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Hexokinase 2 promotes tumor development and progression.American journal of cancer research · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
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  12. Review
  13. The PI3K/Akt Pathway and Glucose Metabolism: A Dangerous Liaison in Cancer.International journal of biological sciences · 2024
    Review
  14. Review
  15. Article
  16. The RNA mCell death & disease · 2022
    Review
  17. Article
  18. Review
  19. Review
  20. Article
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

9 authors at 1 institution in 2 countries.

Kun FanDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, P.R. China.
Zhiyao FanDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, P.R. China.
He ChengDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, P.R. China.
Qiuyi HuangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, P.R. China.
Chao YangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, P.R. China.
Kaizhou JinDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, P.R. China.
Guopei LuoDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, P.R. China.
Xianjun YuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, P.R. China.ORCID 0000-0002-6697-7143
Chen LiuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, P.R. China.
Shanghai Medical College of Fudan University · CN

Funding

National Natural Science Foundation of China 81370065National Natural Science Foundation of China 81372653National Natural Science Foundation of China 81802751National Science Fund for Distinguished Young Scholars 81625016Science and Technology Commission of Shanghai Municipality 15JC1401200
6 · The paper itself

Abstract

Gemcitabine (GEM) is the standard chemotherapy drug for pancreatic cancer. Because of widespread drug resistance, the effect is limited. Therefore, it is urgent to reveal the underlying mechanism. Glycolysis is the most remarkable character of tumor aberrant metabolism, which plays vital roles on tumor drug resistance. Hexokinase 2 (HK2), as the key enzyme regulating the first-step reaction of glycolysis, is overexpressed in many kinds of tumors. The putative role of HK2 resisting GEM therapy was investigated in this study. We found that HK2 was overexpressed in pancreatic cancer and associated with poor prognosis. HK2 knockdown decreased pancreatic cancer cell proliferation, migration viability, and promoted cell apoptosis in vitro. HK2 high expression in pancreatic cancer showed GEM resistance. HK2 knockdown increased the sensitivity of pancreatic cancer cell to GEM, the growth of xenograft tumor with HK2 knockdown was also further decreased with the GEM treatment compared with control in vivo. GEM-resistant pancreatic cancer showed the increase of HK2 dimer rather than HK2 mRNA or protein. Our study revealed that the ROS derived from GEM promoted HK2 dimerization combining with voltage-dependent anion channel, which resulted in the resistance to GEM. Meanwhile, our study established a new sight for GEM resistance in pancreatic cancer.

Indexed as

Drug Resistance, NeoplasmAnimalsAntimetabolites, AntineoplasticApoptosisCell Line, TumorCell MovementCell ProliferationDeoxycytidineDimerizationGemcitabineHexokinaseHumansMaleMiceMice, Inbred BALB CMice, NudeAntimetabolites, AntineoplasticDeoxycytidineGemcitabineHexokinaseVoltage-Dependent Anion ChannelsGEM resistanceHK2 dimerpancreatic cancerROSVDAC

Identifiers

PMID31426130
PMCPMC6792491
OpenAlexW2969381435

What OpenQuestion holds

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LicenceCC BY
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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.