Evidence map›Paper›PMID 28740555›Full record

ArticleTheranostics2017

Atg9b Deficiency Suppresses Autophagy and Potentiates Endoplasmic Reticulum Stress-Associated Hepatocyte Apoptosis in Hepatocarcinogenesis.

Ning Wang, Hor-Yue Tan, Sha Li, Yibin Feng

Open access · goldAbstract read
In one paragraph

Article in Theranostics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
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  10. Enhanced Sensitivity of A549 Cells to Doxorubicin with WSInternational journal of molecular sciences · 2024
    Article
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  13. Journal of clinical and translational hepatology · 2023
    Article
  14. Review
  15. Article
  16. Review
  17. Lysosomal-associated membrane protein family member 5 promotes the metastatic potential of gastric cancer cells.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022
    Article
  18. Review
  19. Review
  20. Autophagy in the Neuronal Ceroid Lipofuscinoses (Batten Disease).Frontiers in cell and developmental biology · 2022
    Review
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

4 authors at 2 institutions in 2 countries.

Ning WangSchool of Chinese Medicine, The University of Hong Kong, Hong Kong S.A.R, PR of China.
Hor-Yue TanSchool of Chinese Medicine, The University of Hong Kong, Hong Kong S.A.R, PR of China.
Sha LiSchool of Chinese Medicine, The University of Hong Kong, Hong Kong S.A.R, PR of China.
Yibin FengSchool of Chinese Medicine, The University of Hong Kong, Hong Kong S.A.R, PR of China.
Chinese University of Hong Kong · CNUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to investigate the mechanism underlying autophagy deficiency during hepatic carcinogenesis. For this purpose, we used choline-deficient, amino acid-defined (CDAA) hepatocarcinogenesis model in mice. miRNA microarrays combined with computational target predictions and GO analysis were used to identify molecular processes involved in carcinogenesis. PCR profiler array was employed to detect the dysregulated autophagy-related genes during carcinogenesis. We observed induction of hepatic tumours with increased inflammation, DNA damage, and cell death. These cellular processes were particularly detected upon oncogenic transformation of hepatocytes in which ER stress was excessively induced. Microarray combined with GO analysis showed that transformation of hepatocytes resulted in dysregulated events associated with cytoplasmic vesicle formation, which, in turn, was related to ER stress-induced autophagy. Defects of autophagy were observed in livers harbouring tumours and suffered a loss of expression of autophagy-related protein 9b (Atg9b). Hepatocytes lacking Atg9b were vulnerable to cell death induced by ER stress stimulus mainly caused by accumulation of ubiquitinated proteins. Loss of Atg9b also blocked recruitment of p62-associated ubiquitinated protein for autophagosome-lysosome degradation as Atg9b-driven phagophores may facilitate docking of both LC3 and p62 to initiate autophagy-associated degradation. miR-3091-3p from tumour-derived exosomes, which were internalised by hepatocytes, could suppress Atg9b expression. Observations from this study advance our knowledge about the regulation of autophagy during hepatocarcinogenesis.

Indexed as

ApoptosisAutophagyEndoplasmic Reticulum StressAnimalsAutophagy-Related ProteinsCarcinogenesisComputational BiologyDisease Models, AnimalDNA DamageGene Expression ProfilingHepatocytesInflammationLiver NeoplasmsMembrane ProteinsMiceMicroarray AnalysisAtg9b protein, mouseAutophagy-Related ProteinsMembrane ProteinsMicroRNAsAtg9bAutophagyER stressHepatic carcinogenesismicroRNA.Tumour-derived exosome

Identifiers

PMID28740555
PMCPMC5505064
OpenAlexW2621501951

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.