Evidence map›Paper›PMID 26048020›Full record

ArticleDigestive diseases and sciences2015

Lysyl Oxidase Is Predictive of Unfavorable Outcomes and Essential for Regulation of Vascular Endothelial Growth Factor in Hepatocellular Carcinoma.

Jiye Zhu, Shan Huang, Guobin Wu, Chaoyuan Huang, Xianjian Li, Zhigang Chen, Lei Zhao, Yinnong Zhao

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

19 citing papers in PubMed, 45 citations in OpenAlex.

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  10. The prognostic value of the lysyl oxidase family in ovarian cancer.Journal of clinical laboratory analysis · 2020
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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

8 authors at 1 institution in 1 country.

Jiye ZhuDepartment of Hepatobiliary Surgery, Guangxi Tumor Hospital, Nanning, 530000, People's Republic of China.
Shan HuangDepartment of Hepatobiliary Surgery, Guangxi Tumor Hospital, Nanning, 530000, People's Republic of China.
Guobin WuDepartment of Hepatobiliary Surgery, Guangxi Tumor Hospital, Nanning, 530000, People's Republic of China.
Chaoyuan HuangDepartment of Hepatobiliary Surgery, Guangxi Tumor Hospital, Nanning, 530000, People's Republic of China.
Xianjian LiDepartment of Hepatobiliary Surgery, Guangxi Tumor Hospital, Nanning, 530000, People's Republic of China.
Zhigang ChenDepartment of Hepatobiliary Surgery, Guangxi Tumor Hospital, Nanning, 530000, People's Republic of China.
Lei ZhaoDepartment of Hepatobiliary Surgery, Guangxi Tumor Hospital, Nanning, 530000, People's Republic of China.
Yinnong ZhaoDepartment of Hepatobiliary Surgery, Guangxi Tumor Hospital, Nanning, 530000, People's Republic of China. mike106210mh@126.com.
Tumor Hospital of Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLysyl oxidase (LOX) is frequently overexpressed in a variety of malignancies and involved in tumor invasion and metastasis. Furthermore, it has been shown that LOX is closely related to vascular endothelial growth factor (VEGF).

aimsIn this study, we aimed to investigate the exact role of LOX and the correlation between LOX and VEGF in hepatocellular carcinoma (HCC).

methodsThe expression levels of LOX in HCC tissue and adjacent noncancerous tissue were evaluated by quantitative reverse transcription polymerase chain reaction and immunohistochemical analysis. The effect of LOX knockdown on cell proliferation, migration, and invasion was investigated in vitro. The role of LOX in the regulation of VEGF was further characterized in HCC cells that had been treated with transforming growth factor beta (TGF-β).

resultsOur study showed that LOX was up-regulated in HCC cell lines and tissue. HCC patients with elevated expression of LOX had relatively shorter disease-free survival and overall survival. Knockdown of LOX reduced the proliferation, migration, and invasion of HCC cells. Additionally, the expression level of LOX positively correlated with that of VEGF. After treatment with TGF-β, the levels of LOX and VEGF were both up-regulated in a dose-dependent manner. In the cells treated with siRNA of LOX, levels of VEGF and phosphorylated p38 were significantly decreased and could not be up-regulated by TGF-β. Inhibition of p38 MAPK signaling abrogated TGF-β-mediated up-regulation of VGEF but did not affect LOX expression.

conclusionsLOX appears to be a predictor of less favorable outcomes and may regulate the expression of VEGF via p38 MAPK signaling.

Indexed as

Gene Expression Regulation, NeoplasticAgedBiopsy, NeedleBlotting, WesternCarcinoma, HepatocellularCell ProliferationDisease-Free SurvivalFemaleHumansImmunohistochemistryKaplan-Meier EstimateLiver NeoplasmsMaleMiddle AgedMultivariate AnalysisPredictive Value of TestsProtein-Lysine 6-OxidaseVascular Endothelial Growth Factor AHepatocellular carcinomaLysyl oxidaseTransforming growth factor betaVascular endothelial growth factor

Identifiers

PMID26048020
OpenAlexW599262067

What OpenQuestion holds

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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.