Evidence map›Paper›PMID 33215807›Full record

ArticleCancer science2021

ECT2 promotes lung adenocarcinoma progression through extracellular matrix dynamics and focal adhesion signaling.

Zeinab Kosibaty, Yoshihiko Murata, Yuko Minami, Masayuki Noguchi, Noriaki Sakamoto

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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  5. Cancers · 2025
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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

5 authors at 2 institutions in 2 countries.

Zeinab KosibatyDepartment of Pathology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.ORCID https://orcid.org/0000-0002-3527-762X
Yoshihiko MurataDepartment of Pathology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Yuko MinamiDepartment of Pathology, National Hospital Organization, Ibaraki Higashi National Hospital, Ibaraki, Japan.
Masayuki NoguchiDepartment of Pathology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Noriaki SakamotoDepartment of Pathology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
University of Tsukuba · JPNational Hospital Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LAC) is the most prevalent form of lung cancer. Epithelial cell transforming sequence 2 (ECT2) is a guanine nucleotide exchange factor that has been implicated in oncogenic and malignant phenotypes of LAC. Here, we identified an oncogenic role of ECT2 in the extracellular matrix (ECM) dynamics of LAC cells. We showed that suppression of ECT2 decreased adhesion and spreading of LAC cells on ECM components. Morphologically, ECT2-depleted cells exhibited a rounded shape and cytoskeletal changes. Examination of transcriptional changes by RNA sequencing revealed a total of 1569 and 828 genes whose expressions were altered (absolute fold change and a difference of >2 fold) in response to suppression of ECT2 in two LAC cells (Calu-3 and NCI-H2342), respectively, along with 298 genes that were common to both cell lines. Functional enrichment analysis of common genes demonstrated a significant enrichment of focal adhesions. In accord with this observation, we found that ECT2 suppression decreased the expression level of proteins involved in focal adhesion signaling including focal adhesion kinase (FAK), Crk, integrin β1, paxillin, and p130Cas. FAK knockdown leads to impaired cell proliferation, adhesion, and spreading of LAC cells. Moreover, in LAC cells, ECT2 binds to and stabilizes FAK and is associated with the formation of the focal adhesions. Our findings provide new insights into the underlying role of ECT2 in cell-ECM dynamics during LAC progression and suggest that ECT2 could be a promising therapeutic avenue for lung cancer.

Indexed as

Adenocarcinoma of LungCell AdhesionCell Line, TumorCell MovementCell ProliferationDisease ProgressionExtracellular MatrixFocal Adhesion Protein-Tyrosine KinasesFocal AdhesionsGene Expression Regulation, NeoplasticHumansLung NeoplasmsProto-Oncogene ProteinsECT2 protein, humanFocal Adhesion Protein-Tyrosine KinasesProto-Oncogene ProteinsECT2extracellular matrixfocal adhesionlung adenocarcinomaRNA sequencing

Identifiers

PMID33215807
PMCPMC7893990
OpenAlexW3100768144

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.