Evidence map›Paper›PMID 34590580›Full record

ArticleeLife2021

Localization of KRAS downstream target ARL4C to invasive pseudopods accelerates pancreatic cancer cell invasion.

Akikazu Harada, Shinji Matsumoto, Yoshiaki Yasumizu, Kensaku Shojima, Toshiyuki Akama, Hidetoshi Eguchi, Akira Kikuchi

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Implications of ADP-Ribosylation Factor-Like Protein 4C (ARL4C) in Human Neoplasia With Special Emphasis on Ameloblastoma: A Scoping Review.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026
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  8. BRAT1 - a new therapeutic target for glioblastoma.Cellular and molecular life sciences : CMLS · 2025
    Article
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  11. Wnt/β-catenin signaling pathway in liver biology and tumorigenesis.In vitro cellular & developmental biology. Animal · 2024
    Review
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  15. Review
  16. Phosphorylation of Arl4A/D promotes their binding by the HYPK chaperone for their stable recruitment to the plasma membrane.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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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

7 authors at 2 institutions in 2 countries.

Akikazu HaradaDepartment of Molecular Biology and Biochemistry, Graduate School of Medicine, Osaka University, Suita, Japan.ORCID 0000-0002-8123-652X
Shinji MatsumotoDepartment of Molecular Biology and Biochemistry, Graduate School of Medicine, Osaka University, Suita, Japan.ORCID 0000-0003-1804-264X
Yoshiaki YasumizuIntegrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), Osaka University, 2-2 Yamadaoka, Suita, Japan.ORCID 0000-0002-9872-4909
Kensaku ShojimaDepartment of Molecular Biology and Biochemistry, Graduate School of Medicine, Osaka University, Suita, Japan.
Toshiyuki AkamaDepartment of Molecular Biology and Biochemistry, Graduate School of Medicine, Osaka University, Suita, Japan.
Hidetoshi EguchiGastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.
Akira KikuchiDepartment of Molecular Biology and Biochemistry, Graduate School of Medicine, Osaka University, Suita, Japan.ORCID 0000-0003-3378-9522
The University of Osaka · JPSalk Institute for Biological Studies · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer has a high mortality rate due to metastasis. Whereas KRAS is mutated in most pancreatic cancer patients, controlling KRAS or its downstream effectors has not been succeeded clinically. ARL4C is a small G protein whose expression is induced by the Wnt and EGF-RAS pathways. In the present study, we found that ARL4C is frequently overexpressed in pancreatic cancer patients and showed that its localization to invasive pseudopods is required for cancer cell invasion. IQGAP1 was identified as a novel interacting protein for ARL4C. ARL4C recruited IQGAP1 and its downstream effector, MMP14, to invasive pseudopods. Specific localization of ARL4C, IQGAP1, and MMP14 was the active site of invasion, which induced degradation of the extracellular matrix. Moreover, subcutaneously injected antisense oligonucleotide against ARL4C into tumor-bearing mice suppressed metastasis of pancreatic cancer. These results suggest that ARL4C-IQGAP1-MMP14 signaling is activated at invasive pseudopods of pancreatic cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticADP-Ribosylation FactorsAgedAged, 80 and overAnimalsFemaleHumansMaleMiceMiddle AgedNeoplasm InvasivenessPancreatic NeoplasmsProto-Oncogene Proteins p21(ras)PseudopodiaTumor Cells, CulturedADP-Ribosylation FactorsARL4C protein, humanKRAS protein, humanProto-Oncogene Proteins p21(ras)ARL4Ccancer biologycell biologyhumaninvasionpancreatic cancer

Identifiers

PMID34590580
PMCPMC8598236
OpenAlexW3202626732

What OpenQuestion holds

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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.