Evidence map›Paper›PMID 33280610›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

Mitophagy promotes sorafenib resistance through hypoxia-inducible ATAD3A dependent Axis.

Hong Wu, Tao Wang, Yiqiang Liu, Xin Li, Senlin Xu, Changtao Wu, Hongbo Zou, Mianfu Cao, Guoxiang Jin, Jinyi Lang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. Review
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025
    Review
  12. Article
  13. Hepatocellular carcinoma drug resistance models.Cancer cell international · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Arctigenin Suppresses MelanomaCurrent cancer drug targets · 2025
    Article
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  19. Review
  20. Article

9 more citing papers are in PubMed but not listed here.

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

14 authors at 6 institutions in 1 country.

Hong WuGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, 518055, Shenzhen, China.
Tao WangDepartment of Gastroenterology, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, 400042, P. R. China.
Yiqiang LiuIntegrative Cancer Center&Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610000, P. R. China.
Xin LiDepartment of Experimental Research, The Affiliated Tumor Hospital of Guangxi Medical University, Nanning, 510000, P. R. China.
Senlin XuInstitute of Pathology and Southwest Cancer Center, Southwest Hospital and Key Laboratory of Tumor Immunopathology, Army Medical University (Third Military Medical University), Chongqing, 400042, P. R. China.
Changtao WuIntegrative Cancer Center&Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610000, P. R. China.
Hongbo ZouInstitute of Pathology and Southwest Cancer Center, Southwest Hospital and Key Laboratory of Tumor Immunopathology, Army Medical University (Third Military Medical University), Chongqing, 400042, P. R. China.
Mianfu CaoInstitute of Pathology and Southwest Cancer Center, Southwest Hospital and Key Laboratory of Tumor Immunopathology, Army Medical University (Third Military Medical University), Chongqing, 400042, P. R. China.
Guoxiang JinInstitute of Pathology and Southwest Cancer Center, Southwest Hospital and Key Laboratory of Tumor Immunopathology, Army Medical University (Third Military Medical University), Chongqing, 400042, P. R. China.
Jinyi LangIntegrative Cancer Center&Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610000, P. R. China.
Bin WangDepartment of Gastroenterology, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, 400042, P. R. China.
Baohua LiuGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, 518055, Shenzhen, China. ppliew@szu.edu.cn.
Xiaolin LuoDepartment of Experimental Research, The Affiliated Tumor Hospital of Guangxi Medical University, Nanning, 510000, P. R. China. luoxiaoling67@126.com.
Chuan XuIntegrative Cancer Center&Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610000, P. R. China. xuchuan100@uestc.edu.cn.
Army Medical University · CNSichuan Cancer Hospital · CNSouthwest Hospital · CNTumor Hospital of Guangxi Medical University · CNShenzhen University Health Science Center · CNUniversity of Electronic Science and Technology of China · CN

Funding

National Natural Science Foundation of China 81873048National Natural Science Foundation of China 82004006
6 · The paper itself

Abstract

backgroundThe identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients.

methodsHypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O

resultsWe found a hyperactivated mitophagy regulating by ATAD3A-PINK1/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice.

conclusionsLoss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC.

Indexed as

AnimalsAntineoplastic AgentsATPases Associated with Diverse Cellular ActivitiesCell Line, TumorDrug Resistance, NeoplasmFemaleHumansLiver NeoplasmsMembrane ProteinsMiceMice, Inbred BALB CMice, NudeMitochondrial ProteinsMitophagySorafenibTumor HypoxiaAntineoplastic AgentsATAD3A protein, humanATPases Associated with Diverse Cellular ActivitiesMembrane ProteinsMitochondrial ProteinsSorafenibATAD3AHypoxiaMitophagySorafenib resistance

Identifiers

PMID33280610
PMCPMC7720487
OpenAlexW3110766076

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.