Evidence map›Paper›PMID 37305391›Full record

ArticleOncology research2023

Calcyclin-binding protein contributes to cholangiocarcinoma progression by inhibiting ubiquitination of MCM2.

Yusen Zhang, Liping Liu, Biwei Luo, Honggui Tang, Xiaofang Yu, Shiyun Bao

Open access · bronzeAbstract read
In one paragraph

Article in Oncology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. RANBP9 and RANBP10 cooperate in regulating non-small cell lung cancer proliferation.Journal of experimental & clinical cancer research : CR · 2025
    Article
  2. Article
  3. Regulatory effect of Wnt signaling on mitochondria in cancer: from mechanism to therapy.Apoptosis : an international journal on programmed cell death · 2025
    Review
  4. Article
  5. 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

6 authors at 1 institution in 1 country.

Yusen ZhangDepartment of Hepatobiliary and Pancrease Surgery, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, 518020, China.
Liping LiuDepartment of Hepatobiliary and Pancrease Surgery, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, 518020, China.
Biwei LuoDepartment of Hepatobiliary and Pancrease Surgery, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, 518020, China.
Honggui TangDepartment of Hepatobiliary and Pancrease Surgery, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, 518020, China.
Xiaofang YuDepartment of Hepatobiliary and Pancrease Surgery, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, 518020, China.
Shiyun BaoDepartment of Hepatobiliary and Pancrease Surgery, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, 518020, China.
Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Cholangiocarcinoma (CCA) represents the epithelial cell cancer with high aggressiveness whose five-year survival rate is poor with standard treatment. Calcyclin-binding protein (CACYBP) shows aberrant expression within several malignant tumors, but the role of CACYBP in CCA remains unknown. Methods: Immunohistochemical (IHC) analysis was used to identify CACYBP overexpression in clinical samples of CCA patients. Moreover, its correlation with clinical outcome was revealed. Furthermore, CACYBP's effect on CCA cell growth and invasion was investigated Results: CACYBP showed up-regulation in CCA, which predicts the dismal prognostic outcome. CACYBP had an important effect on in-vitro and in-vivo cancer cell proliferation and migration. Additionally, knockdown of CACYBP weakened protein stability by promoting ubiquitination of MCM2. Accordingly, MCM2 up-regulation partly reversed CACYBP deficiency's inhibition against cancer cell viability and invasion. Thus, MCM2 might drive CCA development by Wnt/β-catenin pathway. Conclusions: CACYBP exerted a tumor-promoting role in CCA by suppressing ubiquitination of MCM2 and activating Wnt/β-catenin pathway, hence revealing that it may be the possible therapeutic target for CCA treatment.

Indexed as

Bile Duct NeoplasmsCholangiocarcinomabeta CateninBile Ducts, IntrahepaticCalcium-Binding ProteinsHumansMinichromosome Maintenance Complex Component 2S100 Calcium Binding Protein A6Ubiquitinationbeta CateninCACYBP protein, humanCalcium-Binding ProteinsMCM2 protein, humanMinichromosome Maintenance Complex Component 2S100 Calcium Binding Protein A6CACYBPCCAPrognosisUbiquitinationWnt/β-catenin pathway

Identifiers

PMID37305391
PMCPMC10229312
OpenAlexW4367021135

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.