Evidence map›Paper›PMID 28713972›Full record

ArticleMolecular medicine reports2017

Expression and subcellular localization of AT motif binding factor 1 in colon tumours.

Hiromi Kataoka, Yutaka Miura, Makoto Kawaguchi, Shugo Suzuki, Yasuyuki Okamoto, Keiji Ozeki, Takaya Shimura, Tsutomu Mizoshita, Eiji Kubota, Satoshi Tanida and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. 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
0.4field-weighted citation impact, top 37% 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, 11 citations in OpenAlex.

  1. Trial
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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 1 institution in 1 country.

Hiromi KataokaDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Yutaka MiuraDepartment of Molecular Neurobiology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Makoto KawaguchiDepartment of Pathology, Niigata Rosai Hospital, Japan Labor Health and Welfare Organization, Joetsu, Niigata 942‑8502, Japan.
Shugo SuzukiDepartment of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Yasuyuki OkamotoDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Keiji OzekiDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Takaya ShimuraDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Tsutomu MizoshitaDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Eiji KubotaDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Satoshi TanidaDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Satoru TakahashiDepartment of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Kiyofumi AsaiDepartment of Molecular Neurobiology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Takashi JohDepartment of Gastroenterology and Metabolism, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
Nagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AT motif binding factor 1 (ATBF1) is a transcriptional regulator that functions as a tumour suppressor to negatively affect cancer cell growth. In the present study four specific polyclonal antibodies against ATBF1 were generated, and the expression and intracellular localization of ATBF1 in colonic mucosae, polyps, adenoma and adenocarcinoma tissue samples were investigated. The four polyclonal antibodies produced were as follows: MB34 and MB49, which recognize the N‑ and C‑terminal fragments of ATBF1, respectively; and D1‑120 and MB44, which recognize the middle fragments of ATBF1 that contain three nuclear localization signals (NLS). In total, 191 colon samples were examined by immunohistochemical analysis. In addition, colon cancer cells were transfected with four ATBF1 expression vectors, and the subcellular localization of each fragment was examined. Normal colon mucosal cells were not observed to express ATBF1. However, a small number of hyperplastic polyps, serrated adenomas and tubular adenomas expressed ATBF1. Colon cancer cells were observed to express D1‑120‑ and MB44‑reactive middle fragments of ATBF1 in their cell nuclei. However, the N‑ and C‑terminal fragments of ATBF1 did not translocate to the nucleus. Transfection of ATBF1 fragments revealed cleavage of the ATBF1 protein and nuclear translocation of the cleaved middle portion containing the NLS. A positive correlation between the cytoplasmic localization of the N‑ and C‑termini of ATBF1, nuclear localization of the middle portion of ATBF1 and malignant cancer cell invasion was observed. In conclusion, the results of the present study suggest that alterations in the expression and subcellular localization of ATBF1, as a result of post‑transcriptional modifications, are associated with malignant features of colon tumours.

Indexed as

Cell DifferentiationCell NucleusColonic NeoplasmsHomeodomain ProteinsHumansIntestinal MucosaProtein TransportStaining and LabelingSubcellular FractionsHomeodomain ProteinsZFHX3 protein, human

Identifiers

PMID28713972
PMCPMC5548027
OpenAlexW2735706139

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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.