Evidence map›Paper›PMID 34696665›Full record

ArticleBioengineered2021

The roles of Y-box-binding protein (YB)-1 and C-X-C motif chemokine ligand 14 (CXCL14) in the progression of prostate cancer via extracellular-signal-regulated kinase (ERK) signaling.

Chen Wang, Na Zhao, Fuyuki Sato, Keiji Tanimoto, Hiroyuki Okada, Yang Liu, Ujjal K Bhawal

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioengineered, 2021. 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
0.2field-weighted citation impact, top 46% 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, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
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 4 institutions in 3 countries.

Chen WangDepartment of Histology, Nihon University School of Dentistry at Matsudo, Chiba, Japan.ORCID 0000-0003-1962-1977
Na ZhaoSichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.ORCID 0000-0001-6948-8698
Fuyuki SatoPathology Division, Shizuoka Cancer Center, Shizuoka, Japan.ORCID 0000-0002-4435-2118
Keiji TanimotoDepartment of Translational Cancer Research, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.ORCID 0000-0003-4912-4197
Hiroyuki OkadaDepartment of Histology, Nihon University School of Dentistry at Matsudo, Chiba, Japan.ORCID 0000-0003-3251-5853
Yang LiuSichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.ORCID 0000-0002-6033-0648
Ujjal K BhawalDepartment of Pharmacology, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences, Chennai, India.ORCID 0000-0002-3746-009X
Nihon University · JPUniversity of Electronic Science and Technology of China · CNHiroshima University · JPShizuoka Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cold-shock protein Y-box-binding protein (YB)-1 regulates the expression of various chemokines and their receptors at the transcriptional level. Expression of the orphan chemokine CXCL14 is repressed by EGF induced signaling. The possible links between EGF-mediated YB-1 and CXCL14 as well as the functions of critical kinase pathways in the progression of prostate cancer have remained unexplored. Here we examined the correlation between YB-1 and CXCL14, and the ERK/AKT/mTOR pathways in prostate cancer. Knockdown of YB-1 decreased cyclinD1 expression with an upregulation of cleaved-PARP in human prostate cancer cells. EGF treatment upregulated phospho-YB-1 expression in a time-dependent manner, while treatment with an ERK inhibitor completely silenced its expression in prostate cancer cells. EGF treatment stimulates CyclinD1 and YB-1 phosphorylation in an ERK-dependent pathway. Positive and negative regulation of YB-1 and CXCL14 was observed after EGF treatment in prostate cancer cells, respectively. EGF rescues cell cycle and apoptosis via the AKT and ERK pathways. Furthermore, YB-1 silencing induces G1 arrest and apoptosis, while knockdown of CXCL14 facilitates cell growth and inhibits apoptosis in prostate cancer cells. YB-1 and CXCL14 were inversely correlated in prostate cancer cells and tissues. A significant association between poor overall survival and High YB-1 expression was observed in human prostate cancer patients. In conclusion, our data reveal the functional relationship between YB-1 and CXCL14 in EGF mediated ERK signaling, and YB-1 expression is a significant prognostic marker to predict prostate cancer.

Indexed as

Disease ProgressionMAP Kinase Signaling SystemApoptosisCell CycleCell Line, TumorChemokines, CXCCyclin D1Epidermal Growth FactorErbB ReceptorsGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene SilencingHumansMaleMiddle AgedPhosphorylationChemokines, CXCCXCL14 protein, humanCyclin D1EGFR protein, humanEpidermal Growth FactorErbB ReceptorsPoly(ADP-ribose) PolymerasesY-Box-Binding Protein 1YBX1 protein, humanCXCL14EGFERK pathwayProstate cancerYB-1

Identifiers

PMID34696665
PMCPMC8809965
OpenAlexW3208710992

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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.