Evidence map›Paper›PMID 36123339›Full record

ArticleCell death & disease2022

The therapeutic effect of KSP inhibitors in preclinical models of cholangiocarcinoma.

Yuanyuan Shi, Xiaowen Cui, Tianyi Jiang, Yufei Pan, Yunkai Lin, Xiaofan Feng, Zhiwen Ding, Chun Yang, Yexiong Tan, Hongyang Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. 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
1.5field-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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Kinesin Spindle Protein (KIF11) in Mitosis and Cancer.International journal of molecular sciences · 2025
    Review
  3. Review
  4. Article
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

11 authors at 4 institutions in 2 countries.

Yuanyuan Shi *International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, the Naval Medical University, Shanghai, 200438, China.
Xiaowen Cui *International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, the Naval Medical University, Shanghai, 200438, China.
Tianyi Jiang *International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, the Naval Medical University, Shanghai, 200438, China.
Yufei PanInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, the Naval Medical University, Shanghai, 200438, China.
Yunkai LinInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, the Naval Medical University, Shanghai, 200438, China.
Xiaofan FengInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, the Naval Medical University, Shanghai, 200438, China.ORCID 0000-0001-7177-6728
Zhiwen DingDepartment of Hepatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Chun YangChildren's Hospital of Soochow University, Suzhou, 215025, China.
Yexiong TanInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, the Naval Medical University, Shanghai, 200438, China.
Hongyang WangInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, the Naval Medical University, Shanghai, 200438, China. hywangk@vip.sina.com.ORCID 0000-0002-4709-3334
Liwei DongInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, the Naval Medical University, Shanghai, 200438, China. dlw@smmu.edu.cn.ORCID 0000-0003-2116-1674
Second Military Medical University · CNCenter for Naval Analyses · USFudan University Shanghai Cancer Center · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholangiocarcinoma (CCA) is an epithelial malignancy with a dismal prognosis owing to limited treatment options. Here, we identified several compound candidates against CCA using a high-throughput drug screen with approved or emerging oncology drugs, among which kinesin spindle protein (KSP) inhibitors showed potent cytotoxic effects on CCA cells. Treatment with KSP inhibitors SB743921 and ARRY520 caused significant tumor suppression in CCA xenograft models in vivo. Mechanistically, KSP inhibitors led to the formation of abnormal monopolar spindles, which further resulted in the mitotic arrest and cell death of CCA cells both in vivo and in vitro. KEGG pathway analysis of transcriptional data confirmed this finding. Moreover, our clinical data as well as the TCGA database showed KIF11 expression was abundant in most CCA tumor specimens and associated with poor outcomes of CCA patients. Our results demonstrate that the therapeutic regimen of KSP inhibitors could be a promising treatment strategy in CCA.

Indexed as

Antineoplastic AgentsBile Duct NeoplasmsCholangiocarcinomaBile Ducts, IntrahepaticHumansKinesinsAntineoplastic AgentsKinesins

Identifiers

PMID36123339
PMCPMC9485230
OpenAlexW4296347301

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.