Evidence map›Paper›PMID 29327288›Full record

ArticleMolecular and cellular biochemistry2018

Expression of PFKFB3 and Ki67 in lung adenocarcinomas and targeting PFKFB3 as a therapeutic strategy.

Xiaoli Li, Jian Liu, Li Qian, Honggang Ke, Chan Yao, Wei Tian, Yifei Liu, Jianguo Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Hypoxia-induced circ_0017521 enhances glycolysis and promotes NSCLC progression via upregulating the PFKFB3/PI3K-AKT pathway.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  4. Review
  5. Targeting Lung Cancer Metabolism: Therapeutic Opportunities and Challenges.Advances in experimental medicine and biology · 2026
    Review
  6. Article
  7. The regulatory roles and clinical significance of glycolysis in tumor.Cancer communications (London, England) · 2024
    Review
  8. Article
  9. Targeting glycolytic pathway in fibroblast-like synoviocytes for rheumatoid arthritis therapy: challenges and opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Observational
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 1 institution in 1 country.

Xiaoli LiDepartment of Pathology, Affiliated Hospital of Nantong University, No. 20 Xisi Road, Nantong, 226001, Jiangsu, People's Republic of China.
Jian LiuDepartment of Chemotherapy, Affiliated Hospital of Nantong University, Nantong, Jiangsu, People's Republic of China.
Li QianDepartment of Pathology, Affiliated Hospital of Nantong University, No. 20 Xisi Road, Nantong, 226001, Jiangsu, People's Republic of China.
Honggang KeDepartment of Respiratory Medicine, Haian County People's Hospital, Affiliated to Nantong University, Nantong, Jiangsu, People's Republic of China.
Chan YaoDepartment of Pathology, Affiliated Hospital of Nantong University, No. 20 Xisi Road, Nantong, 226001, Jiangsu, People's Republic of China.
Wei TianDepartment of Pathology, Affiliated Hospital of Nantong University, No. 20 Xisi Road, Nantong, 226001, Jiangsu, People's Republic of China.
Yifei LiuDepartment of Pathology, Affiliated Hospital of Nantong University, No. 20 Xisi Road, Nantong, 226001, Jiangsu, People's Republic of China. ntdxliuyifei@sina.com.ORCID http://orcid.org/0000-0001-8068-776X
Jianguo ZhangDepartment of Pathology, Affiliated Hospital of Nantong University, No. 20 Xisi Road, Nantong, 226001, Jiangsu, People's Republic of China. 13815212431@163.com.
Nantong University · CN

Funding

Key talents of Medical Science in Jiangsu Province, China No. QNRC2016682Scientific research topic of Jiangsu provincial health and Family Planning Commission, China No. H201626Six talent peaks project in Jiangsu Province, China No. WSN-059the Science Foundation of Nantong City, Jiangsu, China No. MS12015007
6 · The paper itself

Abstract

Phosphofructokinase-2/fructose-2, 6-bisphosphatase 3 (PFKFB3) catalyzes the synthesis of F2,6BP, which is an allosteric activator of 6-phosphofructo-1-kinase (PFK-1): the rate-limiting enzyme of glycolysis. During tumorigenesis, PFKFB3 increases glycolysis, angiogenesis, and tumor progression. In this study, our aim was to investigate the significance of PFKFB3 and Ki67 in human lung adenocarcinomas and to target PFKFB3 as a therapeutic strategy. In this study, we determined the expression levels of PFKFB3 mRNA and proteins in cancerous and normal lung adenocarcinomas by quantitative reverse transcription PCR (qRT-PCR), Western blot analysis, and tissue microarray immunohistochemistry analysis, respectively. In human adenocarcinoma tissues, PFKFB3 and Ki67 protein levels were related to the clinical characteristics and overall survival. Both PFKFB3 mRNA and protein were significantly higher in lung adenocarcinoma cells (all P < 0.05). A high expression of PFKFB3 and Ki67 were associated with the degree of differentiation, TNM staging, lymph node metastasis, and survival. A high expression of PFKFB3 protein was an independent prognostic marker in lung adenocarcinoma. Subsequently, 1-(4-pyridinyl)-3-(2-quinolinyl)-2-propen-1-one (PFK15) was used as a selective antagonist of PFKFB3. Glycolytic flux was determined by measuring glucose uptake, F2,6BP, and lactate production. Cell viability, cell cycle, cell apoptosis, cell migration, and invasion were analyzed by MTT, flow cytometry, Western blot analysis, wound healing assay, and transwell chamber assay. By targeting PFKFB3, it inhibited cell viability and glycolytic activity. It also caused apoptosis and induced cell cycle arrest. Furthermore, the migration and invasion of A549 cells was inhibited. We conclude that PFKFB3 bears an oncogene-like regulatory element in lung adenocarcinoma progression. In the treatment of lung adenocarcinoma, targeting PFKFB3 would be a promising therapeutic strategy.

Indexed as

A549 CellsAdenocarcinomaAdenocarcinoma of LungAdultAgedAged, 80 and overApoptosisBiomarkers, TumorBlotting, WesternCell ProliferationFemaleFructosediphosphatesGlucoseGlycolysisHumansKi-67 AntigenBiomarkers, Tumorfructose 2,6-diphosphateFructosediphosphatesGlucoseKi-67 AntigenLactic AcidPFKFB3 protein, humanPhosphofructokinase-2PyridinesQuinolinesRNA, MessengerA549Ki67Lung adenocarcinomaPFKFB3PrognosisTherapy

Identifiers

PMID29327288
OpenAlexW2783752132

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.