Evidence map›Paper›PMID 31649264›Full record

ArticleCell death & disease2019

ACTL6A regulates follicle-stimulating hormone-driven glycolysis in ovarian cancer cells via PGK1.

Jiawen Zhang, Jing Zhang, Yingze Wei, Qingxian Li, Qingying Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Actin-Like Protein 6A as an Oncogene and Therapeutic Target in Cancer.International journal of medical sciences · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. The Emerging Role of Chromatin Remodeling Complexes in Ovarian Cancer.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Review
  19. Article
  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

5 authors at 4 institutions in 1 country.

Jiawen ZhangDepartment of Obstetrics and Gynecology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China. jwzhang929@163.com.
Jing ZhangDepartment of Integrated Therapy, Shanghai Cancer Center, Fudan University, Shanghai, China.
Yingze WeiDepartment of Pathology, Nantong Tumor Hospital, Nantong, Jiangsu, China.
Qingxian LiDepartment of Gynaecology and Obstetrics, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Qingying WangDepartment of Obstetrics and Gynecology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China. wangqingying@tongji.edu.cn.
Tongji University · CNNantong Tumor Hospital · CNShanghai Medical College of Fudan University · CNShanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enhanced glycolysis has been identified as a hallmark of cancer. As a novel oncogene, ACTL6A is aberrantly amplified in several types of human cancers and has been shown to regulate tumor growth and progression. However, the roles of ACTL6A in the development of ovarian cancer and the regulation of cancer glucose metabolism are mostly unknown. Here we show that ACTL6A is overexpressed in ovarian cancers compared with adjacent non-tumor tissues, and that ACTL6A overexpression correlates with poor prognosis. Silencing of ACTL6A in vitro inhibits proliferation, clonal growth, and migration, and decreases glucose utilization, lactate production, and pyruvate levels of ovarian cancer cells. We found a positive correlation between ACTL6A and PGK1 expression in ovarian cancer tissues. Enforced ACTL6A expression increased PGK1 expression, whereas knockdown of ACTL6A had the opposite effect. Altered ACTL6A expression inhibits the tumorigenicity of ovarian cancer cells in vivo by downregulating PGK1. In addition, the expression of ACTL6A is regulated by follicle-stimulating hormone (FSH) stimulation via PI3K/AKT pathway. Importantly, ACTL6A regulates FSH-enhanced glycolysis in ovarian cancer. Taken together, our findings highlight the critical role of ACTL6A in ovarian cancer development and identify its contribution to glucose metabolism of cancer cells.

Indexed as

ActinsAdultAgedAnimalsCell Line, TumorCell ProliferationChromosomal Proteins, Non-HistoneDisease-Free SurvivalDNA-Binding ProteinsEpithelial-Mesenchymal TransitionFemaleFollicle Stimulating HormoneGene Expression Regulation, NeoplasticGlycolysisHeterograftsHumansActinsACTL6A protein, humanChromosomal Proteins, Non-HistoneDNA-Binding ProteinsFollicle Stimulating HormonePGK1 protein, humanPhosphatidylinositol 3-KinasesPhosphoglycerate KinaseProto-Oncogene Proteins c-akt

Identifiers

PMID31649264
PMCPMC6813335
OpenAlexW2992806163

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.