Evidence map›Paper›PMID 31083460›Full record

ReviewCancers2019

Targeting ATG4 in Cancer Therapy.

Yuanyuan Fu, Zhiying Huang, Liang Hong, Jia-Hong Lu, Du Feng, Xiao-Ming Yin, Min Li

Abstract readReview
In one paragraph

Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
  2. Article
  3. A novel regulatory circuit of ATG4B and SESN3 promotes T cell leukemogenesis.Journal of experimental & clinical cancer research : CR · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. The role of LncRNA-mediated autophagy in cancer progression.Frontiers in cell and developmental biology · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Modulation of autophagy as a therapeutic strategy forFrontiers in cellular and infection microbiology · 2022
    Review
  19. Aging · 2021
    Article
  20. 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

7 authors.

Yuanyuan FuSchool of Pharmaceutical Sciences, Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, Sun Yat-Sen University, Guangzhou, Guangdong 510006, China. fuyy6@mail2.sysu.edu.cn.
Zhiying HuangSchool of Pharmaceutical Sciences, Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, Sun Yat-Sen University, Guangzhou, Guangdong 510006, China. hzhiying@mail.sysu.edu.cn.
Liang HongSchool of Pharmaceutical Sciences, Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, Sun Yat-Sen University, Guangzhou, Guangdong 510006, China. hongliang@mail.sysu.edu.cn.
Jia-Hong LuState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau, China. jiahonglu@umac.mo.
Du FengState Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 511436, China. feng_du@foxmail.com.
Xiao-Ming YinDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA. xmyin@iu.edu.
Min LiSchool of Pharmaceutical Sciences, Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, Sun Yat-Sen University, Guangzhou, Guangdong 510006, China. limin65@mail.sysu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a lysosome-mediated degradation pathway that enables the degradation and recycling of cytoplasmic components to sustain metabolic homoeostasis. Recently, autophagy has been reported to have an astonishing number of connections to cancer, as tumor cells require proficient autophagy in response to metabolic and therapeutic stresses to sustain cell proliferation. Autophagy-related gene 4 (ATG4) is essential for autophagy by affecting autophagosome formation through processing full-length microtubule-associated protein 1A/1B-light chain 3 (pro-LC3) and lipidated LC3. An increasing amount of evidence suggests that ATG4B expression is elevated in certain types of cancer, implying that ATG4B is a potential anticancer target. In this review, we address the central roles of ATG4B in the autophagy machinery and in targeted cancer therapy. Specifically, we discuss how pharmacologically inhibiting ATG4B can benefit cancer therapies.

Indexed as

ATG4ATG4Bautophagycancer therapy

Identifiers

PMID31083460
PMCPMC6562779

What OpenQuestion holds

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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.