Evidence map›Paper›PMID 27462920›Full record

ArticleOncotarget2017

Over-expression of ASIC1a promotes proliferation via activation of the β-catenin/LEF-TCF axis and is associated with disease outcome in liver cancer.

Cheng Jin, Feng-Lai Yuan, Yuan-Long Gu, Xia Li, Min-Feng Liu, Xiao-Min Shen, Bo Liu, Mao-Qun Zhu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. ASIC1a promotes the proliferation of synovial fibroblasts via the ERK/MAPK pathway.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  7. Article
  8. Review
  9. Article
  10. Mechanism and site of action of big dynorphin on ASIC1a.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. ASIC1a mediates the drug resistance of human hepatocellular carcinoma via the CaLaboratory investigation; a journal of technical methods and pathology · 2017
    Article
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.

Cheng JinDepartment of Hepatobiliary Pancreatic Center, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China.
Feng-Lai YuanDepartment of Research Institute, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China.
Yuan-Long GuDepartment of Hepatobiliary Pancreatic Center, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China.
Xia LiDepartment of Research Institute, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China.
Min-Feng LiuDepartment of Hepatobiliary Pancreatic Center, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China.
Xiao-Min ShenDepartment of Hepatobiliary Pancreatic Center, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China.
Bo LiuDepartment of Hepatobiliary Pancreatic Center, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China.
Mao-Qun ZhuDepartment of Hepatobiliary Pancreatic Center, The Third Hospital Affiliated to Nantong University, Wuxi, 214041, Jiangsu, China.
Wuxi Third People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acid-sensing ion channels 1a (ASIC1a) has been reported to promote migration and invasion in liver cancer. However, the clinical significance and molecular mechanism of ASIC1a in liver cancer remain unknown. In the study, we found that ASIC1a is frequently up-regulated in liver cancer tissues. The over-expression of ASIC1a is associated with advanced clinical stage and poor prognosis. The pro-proliferative of ASIC1a is pH dependent. Knockout of ASIC1a by CRISPR/CAS9 inhibited liver cancer cell proliferation and tumorigenicity in vitro and in vivo through β-catenin degradation and LEF-TCF inactivation. Our results indicated a potential diagnostic marker and chemotherapeutic target for liver cancer.

Indexed as

Gene ExpressionSignal TransductionAcid Sensing Ion ChannelsAnimalsApoptosisbeta CateninCell CycleCell Line, TumorCell ProliferationDisease Models, AnimalGene Expression Regulation, NeoplasticGene Knockout TechniquesHeterograftsHumansKaplan-Meier EstimateLiver NeoplasmsAcid Sensing Ion ChannelsASIC1 protein, humanbeta CateninTCF Transcription FactorsASIC1aCRISPR/CAS9liver cancerproliferationβ-catenin

Identifiers

PMID27462920
PMCPMC5432231
OpenAlexW2498677686

What OpenQuestion holds

Textmetadata
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.