Reciprocal expression of trefoil factor-1 and thyroid transcription factor-1 in lung adenocarcinomas.


Journal

Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776

Informations de publication

Date de publication:
Jun 2020
Historique:
received: 15 04 2019
revised: 16 03 2020
accepted: 24 03 2020
pubmed: 3 4 2020
medline: 20 6 2020
entrez: 3 4 2020
Statut: ppublish

Résumé

Molecular targeted therapies against EGFR and ALK have improved the quality of life of lung adenocarcinoma patients. However, targetable driver mutations are mainly found in thyroid transcription factor-1 (TTF-1)/NK2 homeobox 1 (NKX2-1)-positive terminal respiratory unit (TRU) types and rarely in non-TRU types. To elucidate the molecular characteristics of the major subtypes of non-TRU-type adenocarcinomas, we analyzed 19 lung adenocarcinoma cell lines (11 TRU types and 8 non-TRU types). A characteristic of non-TRU-type cell lines was the strong expression of TFF-1 (trefoil factor-1), a gastric mucosal protective factor. An immunohistochemical analysis of 238 primary lung adenocarcinomas resected at Jichi Medical University Hospital revealed that TFF-1 was positive in 31 cases (13%). Expression of TFF-1 was frequently detected in invasive mucinous (14/15, 93%), enteric (2/2, 100%), and colloid (1/1, 100%) adenocarcinomas, less frequent in acinar (5/24, 21%), papillary (7/120, 6%), and solid (2/43, 5%) adenocarcinomas, and negative in micropapillary (0/1, 0%), lepidic (0/23, 0%), and microinvasive adenocarcinomas or adenocarcinoma in situ (0/9, 0%). Expression of TFF-1 correlated with the expression of HNF4-α and MUC5AC (P < .0001, P < .0001, respectively) and inversely correlated with that of TTF-1/NKX2-1 (P < .0001). These results indicate that TFF-1 is characteristically expressed in non-TRU-type adenocarcinomas with gastrointestinal features. The TFF-1-positive cases harbored KRAS mutations at a high frequency, but no EGFR or ALK mutations. Expression of TFF-1 correlated with tumor spread through air spaces, and a poor prognosis in advanced stages. Moreover, the knockdown of TFF-1 inhibited cell proliferation and soft-agar colony formation and induced apoptosis in a TFF-1-high and KRAS-mutated lung adenocarcinoma cell line. These results indicate that TFF-1 is not only a biomarker, but also a potential molecular target for non-TRU-type lung adenocarcinomas.

Identifiants

pubmed: 32237253
doi: 10.1111/cas.14403
pmc: PMC7293082
doi:

Substances chimiques

Biomarkers, Tumor 0
NKX2-1 protein, human 0
TFF1 protein, human 0
Thyroid Nuclear Factor 1 0
Trefoil Factor-1 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2183-2195

Informations de copyright

© 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

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Auteurs

Daisuke Matsubara (D)

Division of Integrative Pathology, Jichi Medical University, Shimotsuke, Japan.
Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Taichiro Yoshimoto (T)

Division of Integrative Pathology, Jichi Medical University, Shimotsuke, Japan.

Manabu Soda (M)

Department of Cellular Signaling, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

Yusuke Amano (Y)

Division of Integrative Pathology, Jichi Medical University, Shimotsuke, Japan.

Atsushi Kihara (A)

Division of Integrative Pathology, Jichi Medical University, Shimotsuke, Japan.

Toko Funaki (T)

Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Takeshi Ito (T)

Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Yuji Sakuma (Y)

Division of Integrative Pathology, Jichi Medical University, Shimotsuke, Japan.

Tomoki Shibano (T)

Department of Thoracic Surgery, Jichi Medical University, Shimotsuke, Japan.

Shunsuke Endo (S)

Department of Thoracic Surgery, Jichi Medical University, Shimotsuke, Japan.

Koichi Hagiwara (K)

Department of Respiratory Medicine, Jichi Medical University, Shimotsuke, Japan.

Shumpei Ishikawa (S)

Department of Genomic Pathology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.

Masashi Fukayama (M)

Human Pathology Department, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

Yoshinori Murakami (Y)

Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Hiroyuki Mano (H)

Division of Cellular Signaling, National Cancer Center Research Institute, Tokyo, Japan.

Toshiro Niki (T)

Division of Integrative Pathology, Jichi Medical University, Shimotsuke, Japan.

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Classifications MeSH