Evidence map›Paper›PMID 32530543›Full record

Observational studyCancer science2020

Aldolase A promotes epithelial-mesenchymal transition to increase malignant potentials of cervical adenocarcinoma.

Yuki Saito, Akira Takasawa, Kumi Takasawa, Tomoyuki Aoyama, Taishi Akimoto, Misaki Ota, Kazufumi Magara, Masaki Murata, Yoshihiko Hirohashi, Tadashi Hasegawa and 3 more

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Cancer science, 2020. 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
3.7field-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

36 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
  5. Review
  6. Article
  7. Chitosan Nanoparticle-Mediated Delivery ofAntioxidants (Basel, Switzerland) · 2024
    Article
  8. Article
  9. Review
  10. The regulatory roles and clinical significance of glycolysis in tumor.Cancer communications (London, England) · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
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  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

13 authors at 1 institution in 1 country.

Yuki SaitoDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Akira TakasawaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID https://orcid.org/0000-0002-3244-1199
Kumi TakasawaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Tomoyuki AoyamaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Taishi AkimotoDepartment of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Misaki OtaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kazufumi MagaraDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Masaki MurataDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Yoshihiko HirohashiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID https://orcid.org/0000-0002-0608-3914
Tadashi HasegawaDepartment of Surgical Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Norimasa SawadaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Tsuyoshi SaitoDepartment of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Makoto OsanaiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID https://orcid.org/0000-0003-1754-252X
Sapporo Medical University · JP

Funding

Japan Society for the Promotion of Science JP17K08697Japan Society for the Promotion of Science JP17K08698Japan Society for the Promotion of Science JP18K15084Japan Society for the Promotion of Science JP19K16561The Suhara Foundation
6 · The paper itself

Abstract

Recent studies have revealed that metabolic reprogramming is closely associated with epithelial-mesenchymal transition (EMT) during cancer progression. Aldolase A (ALDOA) is a key glycolytic enzyme that is highly expressed in several types of cancer. In this study, we found that ALDOA is highly expressed in uterine cervical adenocarcinoma and that high ALDOA expression promotes EMT to increase malignant potentials, such as metastasis and invasiveness, in cervical adenocarcinoma cells. In human surgical specimens, ALDOA was highly expressed in cervical adenocarcinoma and high ALDOA expression was correlated with lymph node metastasis, lymphovascular infiltration, and short overall survival. Suppression of ALDOA expression significantly reduced cell growth, migration, and invasiveness of cervical cancer cells. Aldolase A expression was partially regulated by hypoxia-inducible factor-1α (HIF-1α). Shotgun proteome analysis revealed that cell-cell adhesion-related proteins were significantly increased in ALDOA-overexpressing cells. Interestingly, overexpression of ALDOA caused severe morphological changes, including a cuboidal-to-spindle shape shift and reduced microvilli formation, coincident with modulation of the expression of typical EMT-related proteins. Overexpression of ALDOA increased migration and invasion in vitro. Furthermore, overexpression of ALDOA induced HIF-1α, suggesting a positive feedback loop between ALDOA and HIF-1α. In conclusion, ALDOA is overexpressed in cervical adenocarcinoma and contributes to malignant potentials of tumor cells through modulation of HIF-1α signaling. The feedback loop between ALDOA and HIF-1α could become a therapeutic target to improve the prognosis of this malignancy.

Indexed as

AdenocarcinomaCell Line, TumorCell MovementCell ProliferationCervix UteriDisease-Free SurvivalEpithelial-Mesenchymal TransitionFeedback, PhysiologicalFemaleFructose-Bisphosphate AldolaseGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansHypoxia-Inducible Factor 1, alpha SubunitKaplan-Meier EstimatePrognosisALDOA protein, humanFructose-Bisphosphate AldolaseHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitRNA, Small Interferingaldolase Acervical adenocarcinomaepithelial-mesenchymal transitionhypoxia-inducible factor-1αmetabolic reprogramming

Identifiers

PMID32530543
PMCPMC7419050
OpenAlexW3034763879

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.