Evidence map›Paper›PMID 26493996›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Glucose-regulated protein 94 mediates cancer progression via AKT and eNOS in hepatocellular carcinoma.

Chien-Yu Huang, Uyanga Batzorig, Wan-Li Cheng, Ming-Te Huang, Wei- Yu Chen, Po-Li Wei, Yu-Jia Chang

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Association Between Glucose-related Protein 94 (GRP94) and Colorectal Cancer Location.Medical archives (Sarajevo, Bosnia and Herzegovina) · 2025
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  17. GRP94 overexpression as an indicator of unfavorable outcomes in breast cancer patients.International journal of clinical and experimental pathology · 2018
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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 3 institutions in 2 countries.

Chien-Yu HuangDivision of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.
Uyanga BatzorigMongolian National University of Medical Sciences, Ulaanbaatar, Mongolia.
Wan-Li ChengDepartment of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Ming-Te HuangDivision of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.
Wei- Yu ChenGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Po-Li WeiDepartment of Surgery, College of Medicine, Taipei Medical University, Taipei, Taiwan. poliwei@tmu.edu.tw.
Yu-Jia ChangGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan. r5424012@tmu.edu.tw.
Taipei Medical University · TWTaipei Medical University-Shuang Ho Hospital · TWWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a crucial health issue worldwide. High glucose-regulated protein 94 (GRP94) expression has been observed in different types of cancer, suggesting a link between tumor progression and GRP94 expression. However, the mechanisms underlying the role of GRP94 in HCC progression remain unclear. We used specific small hairpin RNA (shRNA) to manipulate GRP94 expression in HCC cells. Tissue arrays, MTT assays, xCELLigence assays, and in vivo xenograft model were performed to identify clinicopathological correlations and to analyze cell growth. We found that high GRP94 expression reflected a poor response and a lower survival rate. In vitro and in vivo studies showed that silencing GRP94 suppressed cancer progression. Mechanistically, GRP94 knockdown reduced AKT, phospho-AKT, and eNOS levels but did not influence the AMPK pathway. Our results demonstrated that GRP94 is a key molecule in HCC progression that modulates the AKT pathway and eNOS levels. Our findings suggest that GRP94 may be a new prognostic and therapeutic target for HCC.

Indexed as

AMP-Activated Protein KinasesAnimalsCarcinogenesisCarcinoma, HepatocellularCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMembrane GlycoproteinsMiceNitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktXenograft Model Antitumor AssaysAMP-Activated Protein KinasesendoplasminMembrane GlycoproteinsNitric Oxide Synthase Type IIINOS3 protein, humanProto-Oncogene Proteins c-aktAKTeNOSGRP94HCCProliferation

Identifiers

PMID26493996
OpenAlexW2122183468

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.