Evidence map›Paper›PMID 30612524›Full record

ArticleCell cycle (Georgetown, Tex.)2019

CUL4B regulates autophagy via JNK signaling in diffuse large B-cell lymphoma.

Ying Li, Xiangxiang Zhou, Ya Zhang, Juan Yang, Yangyang Xu, Yi Zhao, Xin Wang

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  11. Autophagy and Metabolism in Normal and Malignant Hematopoiesis.International journal of molecular sciences · 2021
    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

7 authors at 1 institution in 1 country.

Ying Lia Department of Hematology , Shandong Provincial Hospital Affiliated to Shandong University , Jinan , Shandong , People's Republic of China.
Xiangxiang Zhoua Department of Hematology , Shandong Provincial Hospital Affiliated to Shandong University , Jinan , Shandong , People's Republic of China.
Ya Zhanga Department of Hematology , Shandong Provincial Hospital Affiliated to Shandong University , Jinan , Shandong , People's Republic of China.
Juan Yanga Department of Hematology , Shandong Provincial Hospital Affiliated to Shandong University , Jinan , Shandong , People's Republic of China.ORCID 0000-0003-2132-1420
Yangyang Xua Department of Hematology , Shandong Provincial Hospital Affiliated to Shandong University , Jinan , Shandong , People's Republic of China.
Yi Zhaoa Department of Hematology , Shandong Provincial Hospital Affiliated to Shandong University , Jinan , Shandong , People's Republic of China.
Xin Wanga Department of Hematology , Shandong Provincial Hospital Affiliated to Shandong University , Jinan , Shandong , People's Republic of China.ORCID 0000-0001-8051-1481
Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant expression of CUL4B was identified in various types of solid cancers. Cumulative evidences support the oncogenic role of CUL4B in cancers, including regulation of cell proliferation and signal transduction. However, its clinical value and potential pathogenic mechanism in diffuse large B-cell lymphoma (DLBCL) have not been described previously. Therefore, we hypothesize that overexpressed CUL4B may contribute to the pathogenesis of DLBCL. The aim of this study is to assess the expression and the biological function of CUL4B in DLBCL progression. In our study, CUL4B overexpression was observed in DLBCL tissues, and its upregulation was closely associated with poor prognosis in patients. Furthermore, the functional roles of CUL4B was detected both in vitro and in vivo. We demonstrated that silencing CUL4B could not only induce cell proliferation inhibition, cell cycle arrest, and motility attenuation of DLBCL cells in vitro, but also decrease tumor growth in DLBCL xenografts mice. In addition, we identified that CUL4B may act as a potent inductor of JNK phosphorylation in regulation of autophagy. Our findings demonstrated a significant role of CUL4B in the development and progression of DLBCL. CUL4B may act as a useful biomarker and a novel therapeutic target in DLBCL.

Indexed as

MAP Kinase Signaling SystemAdultAgedAged, 80 and overAnimalsApoptosisAutophagyCell Line, TumorCell MovementCell ProliferationCullin ProteinsFemaleGene SilencingHeterograftsHumansKaplan-Meier EstimateCUL4B protein, humanCullin Proteinsautophagycell proliferationCullin4bdiffuse large B-cell lymphomasignaling pathway

Identifiers

PMID30612524
PMCPMC6422499
OpenAlexW2910817072

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.