Evidence map›Paper›PMID 38734828›Full record

ArticleOncogene2024

Phosphorylation of FOXK2 at Thr13 and Ser30 by PDK2 sustains glycolysis through a positive feedback manner in ovarian cancer.

Cancan Zhang, Yinyin Xu, Xinyue Zhu, Xueli Zhang, Fengmian Wang, Lipeng Hu, Huan Lu, Chunlin Tao, Kai Xu, Zhigang Zhang and 3 more

Abstract read
In one paragraph

Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Genes & diseases · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
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  7. Review
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.

Cancan Zhang *Fengxian Hospital, The Third School of Clinical Medicine, Southern Medical University, Shanghai, China.
Yinyin Xu *Fengxian Hospital, The Third School of Clinical Medicine, Southern Medical University, Shanghai, China.
Xinyue Zhu *Fengxian Hospital, The Third School of Clinical Medicine, Southern Medical University, Shanghai, China.
Xueli ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-8306-0639
Fengmian WangFengxian Hospital, The Third School of Clinical Medicine, Southern Medical University, Shanghai, China.
Lipeng HuState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-5941-3825
Huan LuFengxian Hospital, The Third School of Clinical Medicine, Southern Medical University, Shanghai, China.
Chunlin TaoFengxian Hospital, The Third School of Clinical Medicine, Southern Medical University, Shanghai, China.
Kai XuDepartment of Gynecologic Oncology, Zhongshan Hospital, Fudan University, Shanghai, China.
Zhigang ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-8965-223X
Dongxue LiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. dxli@shsci.org.
Tingyan ShiDepartment of Gynecologic Oncology, Zhongshan Hospital, Fudan University, Shanghai, China. shi.tingyan@zs-hospital.sh.cn.
Rong ZhangFengxian Hospital, The Third School of Clinical Medicine, Southern Medical University, Shanghai, China. zr18017807609@smu.edu.cn.ORCID 0000-0002-2136-7181

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81974407, 81672587National Natural Science Foundation of China (National Science Foundation of China) 82173242
6 · The paper itself

Abstract

Ovarian cancer is one of the most common gynecological malignant tumors with insidious onset, strong invasiveness, and poor prognosis. Metabolic alteration, particularly aerobic glycolysis, which is tightly regulated by transcription factors, is associated with the malignant behavior of OC. We screened FOXK2 in this study as a key transcription factor that regulates glycolysis in OC. FOXK2 is overly expressed in OC, and poor prognosis is predicted by overexpression. FOXK2 promotes OC cell proliferation both in vitro and in vivo and cell migration in vitro. Further studies showed that PDK2 directly binds to the forkhead-associated (FHA) domain of FOXK2 to phosphorylate FOXK2 at Thr13 and Ser30, thereby enhancing the transcriptional activity of FOXK2. FOXK2 transcriptionally regulates the expression of PDK2, thus forming positive feedback to sustain glycolysis in OC cells.

Indexed as

Cell ProliferationForkhead Transcription FactorsGlycolysisOvarian NeoplasmsPyruvate Dehydrogenase Acetyl-Transferring KinaseAnimalsCell Line, TumorCell MovementFeedback, PhysiologicalFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudePhosphorylationPrognosisForkhead Transcription FactorsPDK2 protein, humanPyruvate Dehydrogenase Acetyl-Transferring Kinase

Identifiers

PMID38734828
PMCPMC11196215

What OpenQuestion holds

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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.