Evidence map›Paper›PMID 33994864›Full record

ArticleInternational journal of biological sciences2021

ARHGAP25 Inhibits Pancreatic Adenocarcinoma Growth by Suppressing Glycolysis via AKT/mTOR Pathway.

Wen-Kuan Huang, Yi Chen, Huafang Su, Tung-Ying Chen, Jiwei Gao, Yaxuan Liu, Chun-Nan Yeh, Shuijie Li

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Unraveling the Predictive Value ofStem cells international · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022
    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

8 authors at 5 institutions in 4 countries.

Wen-Kuan HuangDivision of Hematology-Oncology, Department of Internal Medicine, Chang Gung Memorial Hospital, Linkou; Chang Gung University College of Medicine, 333, Taoyuan, Taiwan.
Yi ChenDepartment of Oncology-Pathology, Karolinska Institutet, BioClinicum J6:30, Karolinska University Hospital, SE-17164 Solna, Sweden.
Huafang SuDepartment of Radiation and Medical Oncology, the First Affiliated Hospital of Wenzhou Medical University, No.2 Fuxue Lane, Wenzhou 325000, Zhejiang, China.
Tung-Ying ChenDepartment of Pathology, MacKay Memorial Hospital, Taipei, Taiwan.
Jiwei GaoDepartment of Oncology-Pathology, Karolinska Institutet, BioClinicum J6:30, Karolinska University Hospital, SE-17164 Solna, Sweden.
Yaxuan LiuDepartment of Oncology-Pathology, Karolinska Institutet, BioClinicum J6:30, Karolinska University Hospital, SE-17164 Solna, Sweden.
Chun-Nan YehDepartment of Surgery and Pancreatic Cancer Team, Chang Gung Memorial Hospital, Linkou; Chang Gung University College of Medicine, 333, Taoyuan, Taiwan.
Shuijie LiDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE-17177 Stockholm, Sweden.
Karolinska Institutet · SEChang Gung University · TWBioClinicum (Russia) · RUMackay Memorial Hospital · TWWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence reveals that the Rho GTPase-activating protein is a crucial negative regulator of Rho family GTPase involved in tumorigenesis. The Rho GTPase-activating protein 25 (ARHGAP25) has been shown to specifically inactivate the Rho family GTPase Rac1, which plays an important role in pancreatic adenocarcinoma (PAAD) progression. Therefore, here we aimed to clarify the expression and functional role of ARHGAP25 in PAAD. The ARHGAP25 expression was lower in PAAD tissues than that in normal pancreatic tissues based on bioinformatics analysis and immunohistochemistry staining. Overexpression of ARHGAP25 inhibited cell growth of AsPC-1 human pancreatic cancer cells in vitro, while opposite results were observed in BxPC-3 human pancreatic cancer cells with ARHGAP25 knockdown. Consistently, in vivo tumorigenicity assays also confirmed that ARHGAP25 overexpression suppressed tumor growth. Mechanically, overexpression of ARHGAP25 inactivated AKT/mTOR signaling pathway by regulating Rac1/PAK1 signaling, which was in line with the results from the Gene set enrichment analysis on The Cancer Genome Atlas dataset. Furthermore, we found that ARHGAP25 reduced HIF-1α-mediated glycolysis in PAAD cells. Treatment with PF-04691502, a dual PI3K/mTOR inhibitor, hampered the increased cell growth and glycolysis due to ARHGAP25 knockdown in PAAD cells. Altogether, these results conclude that ARHGAP25 acts as a tumor suppressor by inhibiting the AKT/mTOR signaling pathway, which might provide a therapeutic target for PAAD.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaAnimalsCarcinogenesisCell CycleCell Line, TumorCell ProliferationCell Transformation, NeoplasticFemaleGlycolysisGTPase-Activating ProteinsHumansMaleMiceMice, Inbred BALB CMice, NudeARHGAP25 protein, humanGTPase-Activating ProteinsMTOR protein, humanOncogene Protein v-aktRNA, NeoplasmTOR Serine-Threonine KinasesAKT/mTOR signalingARHGAP25glycolysispancreatic adenocarcinomaproliferation.

Identifiers

PMID33994864
PMCPMC8120455
OpenAlexW3158857091

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.