Evidence map›Paper›PMID 24905462›Full record

ArticlePloS one2014

Expression and function analysis of mitotic checkpoint genes identifies TTK as a potential therapeutic target for human hepatocellular carcinoma.

Xiao-Dong Liang, Yue-Chu Dai, Zhao-Yun Li, Mei-Fu Gan, Shi-Rong Zhang, Yin-Pan, Hong-Sheng Lu, Xue-Quan Cao, Bei-jia Zheng, Ling-Fen Bao and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

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  7. CFI-402257, a TTK inhibitor, effectively suppresses hepatocellular carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  18. Studying the Role and Molecular Mechanisms ofBioMed research international · 2020
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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 3 institutions in 1 country.

Xiao-Dong LiangAffiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou, First People's Hospital, Hangzhou, China.
Yue-Chu DaiCentral Hospital of Taizhou City, Taizhou, Zhejiang, China.
Zhao-Yun LiCentral Hospital of Taizhou City, Taizhou, Zhejiang, China.
Mei-Fu GanTaizhou Hospital, Wenzhou Medical University Linhai, Zhejiang, China.
Shi-Rong ZhangAffiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou, First People's Hospital, Hangzhou, China.
Yin-PanCentral Hospital of Taizhou City, Taizhou, Zhejiang, China.
Hong-Sheng LuCentral Hospital of Taizhou City, Taizhou, Zhejiang, China.
Xue-Quan CaoCentral Hospital of Taizhou City, Taizhou, Zhejiang, China.
Bei-jia ZhengCentral Hospital of Taizhou City, Taizhou, Zhejiang, China.
Ling-Fen BaoCentral Hospital of Taizhou City, Taizhou, Zhejiang, China.
Dan-Dan WangCentral Hospital of Taizhou City, Taizhou, Zhejiang, China.
Li-Ming ZhangCentral Hospital of Taizhou City, Taizhou, Zhejiang, China.
Sheng-Lin MaAffiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou, First People's Hospital, Hangzhou, China.
Taizhou Central Hospital · CNHangzhou First People's Hospital · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitotic spindle checkpoint (SAC) genes have been considered targets of anticancer therapies. Here, we sought to identify the attractive mitotic spindle checkpoint genes appropriate for human hepatocellular carcinoma (HCC) therapies. Through expression profile analysis of 137 selected mitotic spindle checkpoint genes in the publicly available microarray datasets, we showed that 13 genes were dramatically up-regulated in HCC tissues compared to normal livers and adjacent non-tumor tissues. A role of the 13 genes in proliferation was evaluated by knocking them down via small interfering RNA (siRNA) in HCC cells. As a result, several mitotic spindle checkpoint genes were required for maintaining the proliferation of HCC cells, demonstrated by cell viability assay and soft agar colony formation assay. Then we established sorafenib-resistant sublines of HCC cell lines Huh7 and HepG2. Intriguingly, increased TTK expression was significantly associated with acquired sorafenib-resistance in Huh7, HepG2 cells. More importantly, TTK was observably up-regulated in 46 (86.8%) of 53 HCC specimens. A series of in vitro and in vivo functional experiment assays showed that TTK overexpression promoted cell proliferation, anchor-dependent colony formation and resistance to sorafenib of HCC cells; TTK knockdown restrained cell growth, soft agar colony formation and resistance to sorafenib of HCC cells. Collectively, TTK plays an important role in proliferation and sorafenib resistance and could act as a potential therapeutic target for human hepatocellular carcinoma.

Indexed as

Genes, cdcCarcinoma, HepatocellularCell Cycle ProteinsCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHepatocytesHep G2 CellsHumansLiver NeoplasmsNiacinamidePhenylurea CompoundsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesSorafenibCell Cycle ProteinsNiacinamidePhenylurea CompoundsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesSorafenibTTK protein, human

Identifiers

PMID24905462
PMCPMC4048189
OpenAlexW2047275206

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.