Evidence map›Paper›PMID 27239961›Full record

ArticleOncogenesis2016

An ANCCA/PRO2000-miR-520a-E2F2 regulatory loop as a driving force for the development of hepatocellular carcinoma.

J Huang, J Yang, Y Lei, H Gao, T Wei, L Luo, F Zhang, H Chen, Q Zeng, L Guo

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.4field-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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
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  10. Identification of Potential Diagnostic and Prognostic Pseudogenes in Hepatocellular Carcinoma Based on Pseudogene-miRNA-mRNA Competitive Network.Medical science monitor : international medical journal of experimental and clinical research · 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

10 authors at 3 institutions in 2 countries.

J HuangDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangdong, China.
J YangDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangdong, China.
Y LeiDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangdong, China.
H GaoDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangdong, China.
T WeiDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangdong, China.
L LuoDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangdong, China.
F ZhangDepartment of Dermatology, Zhujiang Hospital, Southern Medical University, Guangdong, China.
H ChenDepartment of Biochemistry and Molecular Medicine, University of California at Davis Cancer Center, Davis, CA, USA.
Q ZengDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangdong, China.
L GuoDepartment of Pathology, Zhujiang Hospital, Southern Medical University, Guangdong, China.
Southern Medical University · CNZhujiang Hospital · CNUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignancies in Asia especially in China. We previously identified that ANCCA/PRO2000 as an important proliferation-associated protein predicted poor prognosis of patients with HCC. However, the molecular mechanisms of ANCCA/PRO2000 leading to hepatocarcinogenesis and progression are still obscure. In the present study, we found that ANCCA/PRO2000 overexpression in HCC specimens correlated with aggressive tumor behavior and poor survival. Furthermore, ANCCA/PRO2000 exerts strong oncogenic function in HCC and promotes cell proliferation by regulating E2F2 expression, a critical cell cycle regulator. Notably, miR-520a is an intermediate regulator between ANCCA/PRO2000 and E2F2. Mechanistically, ANCCA/PRO2000 not only interacts with E2F2 but also negatively regulates miR-520a that inhibits E2F2 to cooperatively promote in vitro and in vivo growth of HCC cells. Moreover, we demonstrated that ANCCA/PRO2000 enhances the migratory capacity of HCC cells partially by suppressing ERO1L and G3BP2 expression. Additional research identified that miR-372, as a prognostic factor for HCC, could directly target ANCCA/PRO2000. Our results suggest the ANCCA/PRO2000-miR-520a-E2F2 regulatory loop as a driving force for HCC development and ANCCA/PRO2000 as a potential therapeutic target for HCC.

Identifiers

PMID27239961
PMCPMC4945746
OpenAlexW2418359107

What OpenQuestion holds

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LicenceCC BY
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.