Evidence map›Paper›PMID 26603518›Full record

ArticleJournal of cancer research and clinical oncology2016

Expression and regulation of CacyBP/SIP in chronic lymphocytic leukemia cell balances of cell proliferation with apoptosis.

Chunling Fu, Yan Wan, Hengliang Shi, Yanqing Gong, Qingyun Wu, Yao Yao, Mingshan Niu, Zhenyu Li, Kailin Xu

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

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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 2 institutions in 1 country.

Chunling FuBlood Diseases Institute, Xuzhou Medical College, Xuzhou, China.
Yan WanBlood Diseases Institute, Xuzhou Medical College, Xuzhou, China.
Hengliang ShiDepartment of Neurosurgery, The Affiliated Hospital of Xuzhou Medical College, Xuzhou, China.
Yanqing GongBlood Diseases Institute, Xuzhou Medical College, Xuzhou, China.
Qingyun WuBlood Diseases Institute, Xuzhou Medical College, Xuzhou, China.
Yao YaoBlood Diseases Institute, Xuzhou Medical College, Xuzhou, China.
Mingshan NiuBlood Diseases Institute, Xuzhou Medical College, Xuzhou, China.
Zhenyu LiDepartment of Hematology, The Affiliated Hospital of Xuzhou Medical College, Xuzhou, China.
Kailin XuBlood Diseases Institute, Xuzhou Medical College, Xuzhou, China. Lihmd@163.com.
Xuzhou Medical College · CNAffiliated Hospital of Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeChronic lymphocytic leukemia (CLL) is the most common leukemia in Western countries, with incidence in Chinese populations also increasing. CLL involves an accumulation of abnormal B cells which result in dysregulation of cell proliferation and apoptosis rates. The calcyclin-binding protein/Siah-1-interacting protein (CacyBP/SIP) plays a pivotal role in tumorigenicity and cell apoptosis. Here, we investigated the function of CacyBP/SIP in CLL cell proliferation and apoptosis.

methodsCacyBP/SIP expression levels were measured in peripheral blood mononuclear cells from 23 Chinese CLL patients and three healthy donors by western blotting. Correlation analysis was performed to assess associations between CacyBP/SIP expression and clinical stage, chromosome abnormalities and zeta-chain-associated protein kinase 70 (ZAP-70) expression. We silenced CacyBP/SIP expression in MEC-1 cells using a lentivirus system and analyzed cell vitality, cell cycle and tumorigenicity. Apoptosis was also analyzed following the upregulation of CacyBP/SIP expression in MEC-1 cells.

resultsDownregulation of CacyBP/SIP expression in CLL patients was negatively correlated with CLL clinical stage, but not with patient sex, age, del(13q14) or del(17q-) presence, or ZAP-70 expression. CacyBP/SIP silencing significantly enhanced cell proliferation and tumorigenicity. CacyBP/SIP silencing promoted accumulation of cells in S phase by upregulation of β-catenin, cyclin D1 and cyclin E, and downregulation of p21. Moreover, CacyBP/SIP overexpression facilitated CLL apoptosis through the activation of pro-caspase-3.

conclusionCacyBP/SIP is a useful indicator of CLL disease processes and plays an important role in sustaining the balance of cell proliferation and apoptosis.

Indexed as

ApoptosisCell ProliferationAnimalsAsian Peoplebeta CateninBlotting, WesternCalcium-Binding ProteinsCaspase 3Cyclin D1Cyclin EDown-RegulationEnzyme ActivationFemaleGene Expression Regulation, NeoplasticGene SilencingHumansbeta CateninCACYBP protein, humanCalcium-Binding ProteinsCaspase 3Cyclin D1Cyclin EApoptosisCacyBP/SIPCLLProliferationTumorigenicity

Identifiers

PMID26603518
PMCPMC11819274
OpenAlexW2175541255

What OpenQuestion holds

Textmetadata
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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.