Evidence map›Paper›PMID 28415608›Full record

ArticleOncotarget2017

Collagen type IV alpha 1 (COL4A1) and collagen type XIII alpha 1 (COL13A1) produced in cancer cells promote tumor budding at the invasion front in human urothelial carcinoma of the bladder.

Makito Miyake, Shunta Hori, Yosuke Morizawa, Yoshihiro Tatsumi, Michihiro Toritsuka, Sayuri Ohnishi, Keiji Shimada, Hideki Furuya, Vedbar S Khadka, Youping Deng and 11 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
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  6. The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025
    Review
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10 more citing papers are in PubMed but not listed here.

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

21 authors at 4 institutions in 2 countries.

Makito MiyakeDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Shunta HoriDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Yosuke MorizawaDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Yoshihiro TatsumiDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Michihiro ToritsukaDepartment of Psychiatry, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Sayuri OhnishiDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Keiji ShimadaDepartment of Pathology, Nara City Hospital, Nara-shi, Nara, 630-8305, Japan.
Hideki FuruyaClinical and Translational Research Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA.
Vedbar S KhadkaBioinformatics Core, Department of Complementary and Integrative Medicine, University of Hawaii John A. Burns School of Medicine, Honolulu, HI 96813, USA.
Youping DengBioinformatics Core, Department of Complementary and Integrative Medicine, University of Hawaii John A. Burns School of Medicine, Honolulu, HI 96813, USA.
Kenta OhnishiDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Kota IidaDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Daisuke GotohDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Yasushi NakaiDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Takeshi InoueDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Satoshi AnaiDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Kazumasa TorimotoDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Katsuya AokiDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Nobumichi TanakaDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Noboru KonishiDepartment of Pathology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Kiyohide FujimotoDepartment of Urology, Nara Medical University, Kashihara-shi, Nara 634-8522, Japan.
Nara Medical University · JPUniversity of Hawaiʻi at Mānoa · USNara City Hospital · JPUniversity of Hawaii Cancer Center

Funding

UH Hilo COP A&RP20GM103466 · NIGMS · UNIVERSITY OF HAWAII AT MANOA · PI Peter R Hoffmann · 2012 to 2026
$60.3M
RESEARCH DESIGN AND BIOSTATISTICS COREU54MD007584 · NIMHD · UNIVERSITY OF HAWAII AT MANOA · PI MOKUAU, NOREEN, SHIRAMIZU, BRUCE T · 2012 to 2018
$21.1M
Small Grants ProgramP30GM114737 · NIGMS · UNIVERSITY OF HAWAII AT MANOA · PI NERURKAR, VIVEK RAMCHANDRA · 2015 to 2022
$8.1M
NIGMS NIH HHS P20 GM103466NIGMS NIH HHS P30 GM114737NIMHD NIH HHS U54 MD007584
6 · The paper itself

Abstract

Current knowledge of the molecular mechanism driving tumor budding is limited. Here, we focused on elucidating the detailed mechanism underlying tumor budding in urothelial cancer of the bladder. Invasive urothelial cancer was pathologically classified into three groups as follows: nodular, trabecular, and infiltrative (tumor budding). Pathohistological analysis of the orthotopic tumor model revealed that human urothelial cancer cell lines MGH-U3, UM-UC-14, and UM-UC-3 displayed typical nodular, trabecular, and infiltrative patterns, respectively. Based on the results of comprehensive gene expression analysis using microarray (25 K Human Oligo chip), we identified two collagens, COL4A1 and COL13A1, which may contribute to the formation of the infiltrative pattern. Visualization of protein interaction networks revealed that proteins associated with connective tissue disorders, epithelial-mesenchymal transition, growth hormone, and estrogen were pivotal factors in tumor cells. To evaluate the invasion pattern of tumor cells in vitro, 3-D collective cell invasion assay using Matrigel was performed. Invadopodial formation was evaluated using Gelatin Invadopodia Assay. Knockdown of collagens with siRNA led to dramatic changes in invasion patterns and a decrease in invasion capability through decreased invadopodia. The in vivo orthotopic experimental model of bladder tumors showed that intravesical treatment with siRNA targeting COL4A1 and COL13A1 inhibited the formation of the infiltrative pattern. COL4A1 and COL13A1 production by cancer cells plays a pivotal role in tumor invasion through the induction of tumor budding. Blocking of these collagens may be an attractive therapeutic approach for treatment of human urothelial cancer of the bladder.

Indexed as

Neoplasm InvasivenessAnimalsCell Line, TumorCollagen Type IVCollagen Type XIIIEpithelial-Mesenchymal TransitionEstrogensFemaleGene Expression Regulation, NeoplasticGrowth HormoneHumansMaleMiceMice, SCIDRNA, Small InterferingUrinary Bladder NeoplasmsCOL4A1 protein, humanCollagen Type IVCollagen Type XIIIEstrogensGrowth HormoneRNA, Small Interferingbladder cancercollageninvasiontumor budding

Identifiers

PMID28415608
PMCPMC5482641
OpenAlexW2600503901

What OpenQuestion holds

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LicenceCC BY
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.