Evidence map›Paper›PMID 28105232›Full record

ArticleOncology letters2016

TRIP13 is expressed in colorectal cancer and promotes cancer cell invasion.

Kenji Kurita, Masao Maeda, Mohammed A Mansour, Toshio Kokuryo, Keisuke Uehara, Yukihiro Yokoyama, Masato Nagino, Michinari Hamaguchi, Takeshi Senga

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

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  16. Disassembly of the Shieldin Complex by TRIP13.Cell cycle (Georgetown, Tex.) · 2020
    Review
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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

9 authors at 1 institution in 1 country.

Kenji KuritaDepartment of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Masao MaedaDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Mohammed A MansourDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Toshio KokuryoDepartment of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Keisuke UeharaDepartment of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Yukihiro YokoyamaDepartment of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Masato NaginoDepartment of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Michinari HamaguchiDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Takeshi SengaDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyroid hormone receptor interactor 13 (TRIP13) is a member of the ATPases associated with various cellular activities family of proteins and is highly conserved in a wide range of species. Recent studies have demonstrated that TRIP13 is critical for the inactivation of the spindle assembly checkpoint and is associated with the progression of certain cancers. In the present study, the role of TRIP13 in colorectal cancer (CRC) was examined. Reverse transcription-quantitative polymerase chain reaction analysis revealed that TRIP13 messenger RNA was highly expressed in multiple CRC tissues. The depletion of TRIP13 in CRC cells suppressed cell proliferation, migration and invasion. To determine whether the catalytic activity of TRIP13 was critical for cancer progression, an inactive mutant of TRIP13 was expressed in CRC cells. The invasion of cancer cells that expressed the mutant TRIP13 was significantly reduced compared with that of the wild type TRIP13-expressing cancer cells. These results indicate that TRIP13 could be a potential target for CRC treatment.

Indexed as

AAA+colorectal cancerinvasionmigrationTRIP13

Identifiers

PMID28105232
PMCPMC5228471
OpenAlexW2546612812

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.