Evidence map›Paper›PMID 34531663›Full record

ArticleOncoTargets and therapy2021

TFF-1 Functions to Suppress Multiple Phenotypes Associated with Lung Cancer Progression.

Kentaro Minegishi, Yoh Dobashi, Hiroyoshi Tsubochi, Koichi Hagiwara, Yuko Ishibashi, Sachiyo Nomura, Ritsuko Nakamura, Yasukazu Ohmoto, Shunsuke Endo

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Trefoil Factor Family: A Troika for Lung Repair and Regeneration.American journal of respiratory cell and molecular biology · 2022
    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

9 authors at 5 institutions in 1 country.

Kentaro MinegishiDepartment of Thoracic Surgery, Saitama Medical Center, Jichi Medical University, Saitama, Japan.
Yoh DobashiDepartment of Medicine, Saitama Medical Center, Jichi Medical University, Saitama, Japan.ORCID 0000-0003-0507-3332
Hiroyoshi TsubochiDepartment of Thoracic Surgery, Saitama Medical Center, Jichi Medical University, Saitama, Japan.
Koichi HagiwaraDivision of Pulmonary Medicine, Department of Medicine, Jichi Medical University, Tochigi, Japan.
Yuko IshibashiDepartment of Breast and Endocrine Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Sachiyo NomuraDepartment of Gastrointestinal Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0003-4293-6205
Ritsuko NakamuraDepartment of Molecular and Cellular Pathology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.ORCID 0000-0001-9192-4740
Yasukazu OhmotoTokushima University Industry-University R&D Startup Leading Institute, Tokushima, Japan.
Shunsuke EndoDepartment of Thoracic Surgery, Saitama Medical Center, Jichi Medical University, Saitama, Japan.
Jichi Medical University · JPKanazawa University · JPNational Center for Global Health and Medicine · JPThe University of Tokyo · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionTrefoil Factor (TFF) is a member of a protein family comprised of three isoforms, of which TFF-1 exhibits antithetical functions; promotion or suppression of cell proliferation, survival and invasion, depending on the cancer type. However, the pathobiological function of TFF-1 in lung carcinoma has been still unclear.

methodsWe examined the expression and secretion of TFF-1 using cultured human lung carcinoma cells by immunoblotting, immunofluorescence, enzyme-linked immunosorbent assay and quantitative real-time PCR analyses. The effects of TFF-1 on various phenotypes were analyzed in two cell lines, including those transfected with cDNA encoding TFF-1. Cell proliferation and death were examined by hemocytometer cell counting and by colorimetric viability/cytotoxicity assay. Cell cycle profile, migration and invasion were also examined by flow cytometry, wound healing assay and Matrigel Transwell assay, respectively. The effect of TFF-1 overexpression was confirmed by additional transfection of TFF-1-specific siRNA.

resultsEndogenous TFF-1 protein expression and secretion into the media were observed exclusively in adenocarcinoma-derived cell lines. Forced overexpression of TFF-1 drove cell cycle transition, while the proliferation decreased by 19% to 25% due to increased cell death. This cell death was predominantly caused by apoptosis, as assessed by the activation of caspase 3/7. Cell migration was also suppressed by 71% to 82% in TFF-1-transfected cells. The suppressive effect of TFF-1 on proliferation and migration was restored by transfection of TFF-1 siRNA. Moreover, invasion was also suppressed to 77% to 83% in TFF-1-transfected cells.

conclusionThese findings reveal that TFF-1 functions as a suppressor of cancer proliferation by induction of apoptosis, cell migration and invasion and thus may provide a synergistic target for potential treatment strategies for human lung carcinoma.

Indexed as

apoptosisgrowth inhibitioninvasionlung carcinoma cellsmigrationTFF-1

Identifiers

PMID34531663
PMCPMC8439977
OpenAlexW3196384780

What OpenQuestion holds

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LicenceCC BY-NC
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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.