Evidence map›Paper›PMID 25848214›Full record

ArticleDrug design, development and therapy2015

Lost expression of ADAMTS5 protein associates with progression and poor prognosis of hepatocellular carcinoma.

Chongyi Li, Yanli Xiong, Xueqin Yang, Lin'ang Wang, Shiheng Zhang, Nan Dai, Mengxia Li, Tao Ren, Yuxin Yang, Shu-Feng Zhou and 2 more

Abstract read
In one paragraph

Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

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  13. ADAMTS-5: A difficult teenager turning 20.International journal of experimental pathology · 2020
    Review
  14. Article
  15. ADAMTS5 acts as a tumor suppressor by inhibiting migration, invasion and angiogenesis in human gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2019
    Article
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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

12 authors.

Chongyi LiCancer Center, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, People's Republic of China ; Department of Biochemistry and Molecular Biology, The Third Military Medical University, Chongqing, People's Republic of China.
Yanli XiongCancer Center, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, People's Republic of China.
Xueqin YangCancer Center, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, People's Republic of China.
Lin'ang WangCancer Center, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, People's Republic of China.
Shiheng ZhangCancer Center, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, People's Republic of China.
Nan DaiCancer Center, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, People's Republic of China.
Mengxia LiCancer Center, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, People's Republic of China.
Tao RenCancer Center, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, People's Republic of China.
Yuxin YangCancer Center, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, People's Republic of China.
Shu-Feng ZhouDepartment of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA.
Lixia GanDepartment of Biochemistry and Molecular Biology, The Third Military Medical University, Chongqing, People's Republic of China.
Dong WangCancer Center, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered expression of ADAMTS5 is associated with human carcinogenesis and tumor progression. However, the role of ADAMTS5 in hepatocellular carcinoma (HCC) is unclear. This study analyzed ADAMTS5 expression in HCC tissues and tested for association with clinicopathological and survival data from HCC patients and then explored the role of ADAMTS5 in HCC cells in vitro. Paraffin blocks from 48 HCC patients were used to detect ADAMTS5 and vascular endothelial growth factor (VEGF) expression and microvessel density (MVD). A normal liver cell line and HCC cell lines were used to detect ADAMTS5 expression and for ADAMTS5 manipulation. ADAMTS5 cDNA was stably transfected into HCC cells and ADAMTS5 expression assessed by Western blot analysis. Tumor cell-conditioned growth medium was used to assess human umbilical vein endothelial cell migration and Matrigel tube formation. Xenograft assay was performed to determine the role of ADAMTS5 in vivo. The data showed that the expression of ADAMTS5 was reduced in HCC, which was inversely associated with VEGF expression, MVD, and tumor size and associated with poor overall survival of HCC patients. Lentivirus-mediated ADAMTS5 expression significantly inhibited tumor angiogenesis by downregulating in vitro expression of VEGF and inhibiting migration and tube formations, and also inhibited tumor growth and VEGF expression and reduced MVD in vivo in a mouse xenograft model. Taken together, these results suggest that ADAMTS5 plays a role in suppression of HCC progression, which could be further studied as a promising novel therapeutic target and a potential prognostic marker in HCC.

Indexed as

Disease ProgressionADAM ProteinsADAMTS5 ProteinAdultAgedAnimalsCarcinoma, HepatocellularCells, CulturedFemaleHep G2 CellsHumansLiver NeoplasmsMaleMiceMicrovesselsMiddle AgedADAM ProteinsADAMTS5 ProteinADAMTS5 protein, humanVascular Endothelial Growth Factor AA disintegrin and metalloproteinase with thrombospondin motifs 5tumor angiogenesistumor cell xenograft

Identifiers

PMID25848214
PMCPMC4378293

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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.