Evidence map›Paper›PMID 38872370›Full record

ArticleCancer medicine2024

Trefoil factor 1 suppresses stemness and enhances chemosensitivity of pancreatic cancer.

Junpei Yamaguchi, Toshio Kokuryo, Yukihiro Yokoyama, Shunsuke Oishi, Masaki Sunagawa, Takashi Mizuno, Shunsuke Onoe, Nobuyuki Watanabe, Atsushi Ogura, Tomoki Ebata

Abstract read
In one paragraph

Article in Cancer medicine, 2024. 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
–field-weighted citation impact
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

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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.

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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

10 authors.

Junpei YamaguchiDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0002-5892-5271
Toshio KokuryoDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0001-7176-7581
Yukihiro YokoyamaDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shunsuke OishiInstitute of Transformative Bio-Molecules, Nagoya University, Nagoya, Japan.
Masaki SunagawaDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Takashi MizunoDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shunsuke OnoeDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nobuyuki WatanabeDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Atsushi OguraDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Tomoki EbataDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Funding

Japan Society for the Promotion of Science JSPS KAKENHI grant number 17K10695Japan Society for the Promotion of Science JSPS KAKENHI grant number 20H03751
6 · The paper itself

Abstract

BACKGROUND AND

aimsPancreatic cancer is one of the most lethal malignancies, partly due to resistance to conventional chemotherapy. The chemoresistance of malignant tumors is associated with epithelial-mesenchymal transition (EMT) and the stemness of cancer cells. The aim of this study is to investigate the availability and functional mechanisms of trefoil factor family 1 (TFF1), a tumor-suppressive protein in pancreatic carcinogenesis, to treat pancreatic cancer.

methodsTo investigate the role of endogenous TFF1 in human and mice, specimens of human pancreatic cancer and genetically engineered mouse model of pancreatic cancer (KPC/TFF1KO; Pdx1-Cre/LSL-KRAS

resultsThe deficiency of TFF1 was associated with increased EMT of cancer cells in mouse models of pancreatic cancer, KPC. The expression of TFF1 in cancer cells was associated with better survival rate of the patients who underwent chemotherapy, and loss of TFF1 deteriorated the benefit of gemcitabine in KPC mice. Extracellular administration of TFF1 inhibited gemcitabine-induced EMT, Wnt pathway activation and cancer stemness, eventually increased apoptosis of pancreatic cancer cells in vitro. In vivo, combined treatment of gemcitabine and subcutaneous administration of TFF1 arrested tumor growth in xenograft mouse model and resulted in the better survival of KPC mice by inhibiting EMT and cancer stemness.

conclusionThese results indicate that TFF1 can contribute to establishing a novel strategy to treat pancreatic cancer patients by enhancing chemosensitivity.

Indexed as

Drug Resistance, NeoplasmNeoplastic Stem CellsPancreatic NeoplasmsTrefoil Factor-1AnimalsApoptosisCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionFemaleGemcitabineGene Expression Regulation, NeoplasticHumansMaleMiceMice, TransgenicGemcitabineTFF1 protein, humanTrefoil Factor-1cancer stem cellchemosensitivityepithelial‐mesenchymal transitionpancreatic cancertrefoil factor

Identifiers

PMID38872370
PMCPMC11176577

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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.