Evidence map›Paper›PMID 34485872›Full record

ArticleiScience2021

FBP17-mediated finger-like membrane protrusions in cell competition between normal and RasV12-transformed cells.

Tomoko Kamasaki, Yumi Miyazaki, Susumu Ishikawa, Kazuya Hoshiba, Keisuke Kuromiya, Nobuyuki Tanimura, Yusuke Mori, Motosuke Tsutsumi, Tomomi Nemoto, Ryota Uehara and 3 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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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

13 authors at 4 institutions in 1 country.

Tomoko KamasakiDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Sapporo, Hokkaido 060-0815, Japan.
Yumi MiyazakiDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Sapporo, Hokkaido 060-0815, Japan.
Susumu IshikawaDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Sapporo, Hokkaido 060-0815, Japan.
Kazuya HoshibaDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Sapporo, Hokkaido 060-0815, Japan.
Keisuke KuromiyaDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Sapporo, Hokkaido 060-0815, Japan.
Nobuyuki TanimuraDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Sapporo, Hokkaido 060-0815, Japan.
Yusuke MoriDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Sapporo, Hokkaido 060-0815, Japan.
Motosuke TsutsumiResearch Institute for Electronic Science, Hokkaido University, Sapporo, Hokkaido 001-0020, Japan.
Tomomi NemotoResearch Institute for Electronic Science, Hokkaido University, Sapporo, Hokkaido 001-0020, Japan.
Ryota UeharaFaculty of Advanced Life Science, Hokkaido University, Sapporo, Hokkaido 001-0021, Japan.
Shiro SuetsuguDivision of Biological Science, Nara Institute of Science and Technology, Ikoma, Nara 630-0192, Japan.
Toshiki ItohDivision of Membrane Biology, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
Yasuyuki FujitaDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Sapporo, Hokkaido 060-0815, Japan.
Hokkaido University · JPNational Institutes of Natural Sciences · JPKobe University · JPNara Institute of Science and Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At the initial stage of carcinogenesis, cell competition often occurs between newly emerging transformed cells and the neighboring normal cells, leading to the elimination of transformed cells from the epithelial layer. For instance, when RasV12-transformed cells are surrounded by normal cells, RasV12 cells are apically extruded from the epithelium. However, the underlying mechanisms of this tumor-suppressive process still remain enigmatic. We first show by electron microscopic analysis that characteristic finger-like membrane protrusions are projected from both normal and RasV12 cells at their interface. In addition, FBP17, a member of the F-BAR proteins, accumulates in RasV12 cells, as well as surrounding normal cells, which plays a positive role in the formation of finger-like protrusions and apical elimination of RasV12 cells. Furthermore, cdc42 acts upstream of these processes. These results suggest that the cdc42/FBP17 pathway is a crucial trigger of cell competition, inducing "protrusion to protrusion response" between normal and RasV12-transformed cells.

Indexed as

Cell biologyOpticsOrganizational aspects of cell biology

Identifiers

PMID34485872
PMCPMC8405961
OpenAlexW3195406945

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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.